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237 Cards in this Set

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Renal Disease
Clinical findings:
May present with no sx or non specific complaints of ________,___________,________
Consequently, many present with advanced dz
More specific sx
HTN
Edema
Polyuria
Hematuria
Dark colored “cola colored” urine
fatigue, malaise, or anorexia
Renal Disease
History:
_________(duration and complications)
____________(duration and complications)
Recurrent ____
Renal ______
Family history of renal dz
Arthralgias, skin rash, fever, and weight loss
Medications
Prescription, OTC, illicit drugs, herbs
Review of records to determine previous renal functions
Diabetes

Hypertension

UTI’s

calculi
Renal Disease
Physical Exam:
Signs of __________ illness responsible for renal dz
__________ exam may suggest HTN, DM, or bacterial endocarditis (_______)
Skin may show edema, rash, purpura
Joints examination for signs of __________
Rectal exam in men and pelvic exam in women to reveal signs of ________________
systemic

Retinal

Roth’s spot

arthritis

urinary obstruction
Renal Disease
GFR:
____________ concentration in serum assesses GFR
Creatinine comes from __________ as a result of muscle breakdown
Daily rate is constant and determined by skeletal muscle mass
Is eliminated by glomerular filtration, and is a marker of renal function
Normal is ______ mg/dl in men, and ______ mg/dl in women (decreased muscle mass in women)
Certain drugs may interfere with creatinine excretion and cause false elevation (4)
Creatinine

creatine

0.8-1.3

0.6-1.1

Cimetidine, trimethoprim, triamterene, amiloride
Renal Disease
BUN:
Urea is product of ________ metabolism
Levels reflect dietary intake and catabolic rate of protein
Excreted by glomerular filtration, but reabsorbed in high ________ states such as volume depletion
So, varies with extra cellular fluid volume, where creatinine usually doesn’t
Ratio of BUN to creatinine is _____
protein

sodium

10:1
Disproportionate Increase in Blood Urea Nitrogen:
Volume depletion "__________"
_____ hemorrhage
Corticosteroid or cytotoxic agents
High-_____ diet
Obstructive uropathy
Sepsis
Catabolic states tissue breakdown

Disproportionate Decrease in Blood Urea Nitrogen:
Low-protein diet
________ disease
prerenal azotemia

GI

protein

Liver
Renal Disease
Creatine Clearance:
Provides a reasonable estimate of GFR
Errors that limit its accuracy are - Increasing creatinine secretion & improper ______ collection
*Normal Ccr in men is ______ mg/kg/day*
*Normal Ccr in women is ______ mg/kg/day*
If it deviates significantly, may be problem with urine collection of 24 hour urine
Cockroft-Gault formula may be a simpler approach if this is a persistant problem
urine

20-25

15-20
Renal Disease
Lab and renal function:
Renal tubular function evaluated by examining kidneys ability to maintain Na+ and H2O balance and acid base balance (urine __)
Fe Na = fractional excretion of sodium in urine useful in the ddx of __________ renal failure (volume depletion vs renal dz)
In polyuric patient, __________ helps determine renal ability to concentrate urine (Diabetes insipidus vs nephrogenic diabetes insipidus)
pH

oliguric

water deprivation test
Renal Disease
Proteinuria:
Normal excretion < ___ mg/day
Transient abnormal proteinuria occurs with (3)
150

Fever
CHF
Exercise
Renal Disease
Proteinuria:
_______________ (benign)
Characterized by lack of protein in urine collected overnight while patient is supine
Orthostatic proteinuria
Renal Disease
Proteinuria:
Persistant proteinuria
Should get timed urine specimen with urine creatinine to help determine accuracy of collection
More than ___ g of protein/day have glomerular dz
Less than 3.5 g of protein/day is glomerular and tubular dz
*_______________(30-300 mg/24h)* associated with renal dz progression and high CV morbidity and mortality in diabetic and hypertensive patients
_________ to creatinine ratio on spot urine can assess the amount of albuminuria with ratio of 30mg/g or higher suggesting microalbuminuria
Need 1st morning urine
3.5

microalbuminuria

Albumen
Renal Disease
Urinalysis: Color
Normal urine is colorless to deep yellow depending on pigment concentration
Abnormal colors may mean ________,__________, pigment, drug, or dye
_______ or __________ results in smoke colored urine
Cloudiness with high concentration of _______, or high amorphous phosphates in alkaline urine
disease, infection

RBC’s or myoglobin

WBC’s
Renal Disease
Urinalysis: Chemistry (dipstick)
pH , hemoglobin, protein, glucose, ketones, leukocyte esterase, nitrites
Protein on dipstick detects only ______, not immunoglobulins or Bence Jones proteins
Concentrated urine may show trace to 1+ protein in normal patients
________ detected is due to hemoglobin or myoglobin
____ and _________ mean infection, but negatives does not rule out infection
albumen

Blood

LE and nitrites
Renal Disease
Urinalysis: Microscopic exam
Test of urine sediment for cells, casts, crystals, and organisms
Microscopic hematuria is > __ rbc/hpf in urine not contaminated by menses
_________ cells are dysmorphic
Non glomerular cells are normal
_______ casts means nephronic origin of blood
2

Glomerular

RBC
Urinalysis: Microscopic exam
_______ is the presence of more than 4 wbc/hpf
Suggests _____ or __________
________ pyuria is pyuria with negative culture~
Prostatitis
Chronic urethritis
Renal tuberculosis
Renal stones
Papillary necrosis
Pyuria

UTI or inflammation

Sterile
Renal Disease
Urinalysis: Microscopic
Eosinophyls on Wrights stain suggests ___________
Renal tubular epi cells are seen in ___________,___________, and ___________
Free fat droplets seen in heavy ___________
interstitial nephritis

acute tubular necrosis, glomerulonephritis, and pyelonephritis

proteinuria
Renal Disease
Urinalysis: Microscopic exam
________ are cylindrical structures from intratubular protein precipitation
RBC’s or WBC casts mean inflammatory ___________ disease
RBC’s alone usually indicates a significant __________ lesion or _______________
Renal tubular cell (course granular) casts in renal failure means acute ___________
Leukocyte casts in infection means _______ rather than cystitis and may also be seen in interstitial nephritis
Casts

parenchymal

glomerular lesion or interstitial nephritis

tubular necrosis

pyelo
Renal Disease
Urinalysis: Microscopic exam
Crystals – Ca oxylate are ________ shaped, and uric acid are _________ shaped
In the absence of sx, have little clinical significance
But, cystine crystals indicate ________
Triple phosphate crystals are in ________ urine
Bacteria in unspun urine means ____
__________ means treat patient and sex partner
envelope

rhomboid

cystinuria

alkaline

UTI

Trichomonas
Acute Nephritic Syndrome:
Abrupt onset of renal dysfunction with _________ that is nephronic in origin (glomerular or tubular in origin)
_____ casts and dysmorphic erythrocytes in urine sediment also highly suggests nephronic origin
Significant _________ also
Caused by inflammation causing dysfunction of the glomerulus (filtering and excretion problems)
hematuria

RBC

proteinuria
Acute Nephritic Syndrome:
Clinical findings- _______ retention leading to HTN, circulatory overload, and CHF

Causes:
Kids- post ___________ glomerulonephritis is the most well known, also ____________ purpura
Adults- SLE, _______ nephritis, vasculitis, infective _________
sodium

streptococcal

Henoch-Scholein

lupus

endocarditis
Nephrotic Syndrome:
Increased glomerular __________ resulting in proteinuria of >3.5g/d/1.73m2 body surface area with~ (3)`
permeability

Edema
Hypoalbuminemia
Hyperlipidemia
Nephrotic syndrome:
Proteinuria charactistic of both nephritic and nephrotic syndrome
However on urinalysis
Nephrotic syndrome has:
_____ fat bodies
Course granular ______
Cellular elements
But lack the “______” sediment of nephritic syndrome
Oval

casts

active
Nephrotic Syndrome:
Causes-
Membranous nephropathy
____
_________ nephropathy
Multiple myeloma
__________(abnormal deposition of protein called amyloid into tissues causing serious harm in some organs, no harm in others)
SLE

Diabetic

Amyloidosis
Rapidly progressive renal failure:
Rapid deterioration of renal function over weeks to months
Causes-
_________ uropathy
Malignant ________
____ with hemolytic uremic syndrome
Bilateral __________
Multiple myeloma
Rapidly progressive glomerulonephritis
Obstructive

hypertension

TTP

renal artery stenosis
Acute Renal Failure:
Abrupt decline in renal function over days to weeks
Causes-
Decreased renal blood flow
(____________)
Intrinsic parenchymal disease (_________)
Obstruction to urine flow (____________)
pre-renal azotemia

renal azotemia

post renal azotemia
Tubulointerstitial nephropathy:
Glomeruli and vasculture are spared but the _________ and __________ are affected
Can be classified as acute interstitial nephropathy or chronic interstitial nephropathy depending on how quickly renal dysfunction progresses
interstitium and tubules
Tubointerstitial nephropathy:
Chronic characterized by
_____ insufficiency
__________ range proteinuria
Severe tubular damage
Significant ________ wasting, hyperkalemia and metabolic __________ even with modest renal insufficiency
Renal

Non nephrotic

sodium

acidosis
Tubointerstitial nephropathy:
Acute characterized by
Usually caused by _____
Sudden onset of signs of renal dysfunction
____________ cell infiltrates in renal interstitium
Important in the ddx of ____________
drug

Inflammatory

acute renal failure
Urinary Tract Imaging
Renal ________:
Useful for the detection of renal masses, cysts, and dilation of collecting system (____________)
In unexplained renal failure can help assess size and __________ uropathy
In renal failure, US showing ________ kidneys suggests chronic renal failure where _______ size suggests acute renal failure or chronic renal failure caused by DM, amyloidosis, or multiple myeloma
Ultrasound

hydronephrosis

obstructive

small

normal
Urinary Tract Imaging
Renal Ultrasound:
_________ US with doppler imaging detects disease of major _____________
Simple _________ identified by US
Kidney size on ultrasound with a discrepancy of more than ___ cm may suggest renovascular disease
Duplex

renal arteries or veins

cysts

1.5
Urinary Tract Imaging
____________:
IV administration of contrast medium that is excreted through the kidney through glomerulo filtration
Nephrogram image produced due to contrast medium concentrating in the renal tubules
When it passes through the collecting system, the calyces, renal pelvis, ureters, and bladder are seen

Advantage is you can see the site and cause of obstruction and detect __________ or calyceal blunting
Disadvantage, contrast medium can cause ____________ especially in patient with renal insufficiency, volume depletion, diabetes, or multiple myeloma
IVP (intravenous pyelography)

papillary necrosis

nephrotoxicity
Urinary Tract Imaging
Retrograde Pyelography:
Contrast material injected into _________ at time of cystoscopy
Helpful in defining __________ in the ureter or renal pelvis, especially with non visualized kidney on IVP
Stones can be moved during this procedure using _______
ureter

obstruction

basket
Urinary Tract Imaging
CT of the Kidney:
Usually done with contrast medium
Helpful in evaluation of ______,________, perinephric pathology
Helpful in vascular pathology such as __________
Used to guide kidney ________, or collection of fluid as in aspiration of ____________
masses, cysts

renal vein thrombosis

biopsy

perinephric abcess
Urinary Tract Imaging
_______:
Helpful in evaluating complex masses, staging tumors, detecting invasion of renal veins
Diagnosing renovascular disease in lieu of CT in patients with renal failure to avoid use of contrast material

_______ has inhanced the detection and hemodynamic significance of renal artery stenosis
Cannot be used in people with _________ or other ferromagnetic devices
MRI

MRA (magnetic resonance angiography)

pacemakers
Urinary Tract Imaging
___________:
Injection of contrast media into the aorta and renal arteries to see renal vasculature
Helpful in renal artery stenosis, thrombosis, or renal mass
Important in the workup of _________
Used to look for microaneurysms in polyarteritis nodosa
Renal arteriography

kidney donors
Urinary Tract Imaging
Radionuclide imaging:
IV radiolabeled compounds
Images taken with gamma camera
Used in evaluation of
___________ problems
Renovascular _________
GFR estimation
Pyelonephritis/renal abcess
Interstitial nephritis
__________
Renal perfusion

hypertension

obstruction
Renal Biopsy:
Performed when glomerular lesion suspected or unexplained acute renal failure
____________ bx most commonly done
Complications are __________, renal hematoma, laceration with development of av fistula, accidental _______ of liver, spleen or bowel
Percutaneous

hematuria

biopsy
nephrotic sydrome
persistent proteinuria
hematuria asso w/ abnormal urine sediment or proteinuria
unexplained hematuria after exclusion of lower urinary tract cause
systemic disorders w/ kidney involvement
acute renal failure (atypical features or failure to recover in 6 wk)
rapidly progressive renal failure
renal allograft dysfunction
Indications for kidney biopsy
Capillary bed that recieves blood from afferent arteriole and drains by efferent arteriole
4 cell types
Visceral epithelial (podocyte)
Endothelial
Mesangial cell
Parietal epithelial
Glomerulus
__________ supports the GBM by trebecular network

_________ provides skeletal framework to capillary network and controls blood flow of glomerular capillaries in response to different mediators

__________ line the capillary lumen

________ covers interior of bowman's capsule
epithelial

mesangium

endothelial

parietal epithelium
Clinical manifestations of glomerular disease:

Urinary abnormalities
__________ and ___________

Nonspecific systemic symptoms
_______,_________,________

Altered glomerular function
Changes in GBM permeability causing ___________(protein filtered based on size, shape and electrical charge, less than 50mg/day in urine)

Decreased GFR due to abnormal filtration
Increased BUN and Creatinine
Proteinuria and hematuria

Hypertension, edema, malaise

proteinuria
Clinical manifestations of glomerular disease:
RBC casts or dysmorphic RBC’s means nephronal bleeding and characteristic of ______________
RBC casts sometimes seen in acute ______________
Renal _____ retention is common in GN and causes:
Edema
Volume overload
CHF
HTN
glomerulonephritis

interstitial nephritis

salt
Nephritic Syndrome:
Abrupt onset of _________ with RBC casts
__________(non-nephrotic range)
Temporary impairment of renal function with oliguria, increased BUN and Creatinine
Salt and water retention and ______
Most commonly due to proliferative GN, protoype being _____________
hematuria

Proteinuria

HTN

PSGN (post streptococcal glomerulonephritis)
PSGN:
Postinfectious complication of _________ infection
Strept throat leads to PSGN in fewer than 5% of those not treated (within 7-28 days)
More common in ________(up to 50% in some accounts)
Typically in kids aged 3-12, but can occur in adults
GABHS

impetigo
PSGN:
Symptoms and signs-
________,__________,________

Laboratory findings-
Low serum ___________ levels
ASO titers high
_______ colored urine with RBC’s and RBC cast
Proteinuria less than 3.5 g/dl (_________)
Microscopy shows diffuse proliferative glomerulonephritis
Immunoflorescence shows ____ and C3 along the mesangium and capillary basement membrane
Oliguria, edema, hypertension

complement

Cola

non-nephrotic

IgG
PSGN:
Treatment-
_________
Appropriate __________
____________ and salt restriction if needed
_________ not helpful
Supportive

antibiotics

Antihypertensives

Steroids
PSGN:
Prognosis-
Very favorable in children
Less than 5% of adults will develop _______________ and smaller percentage will develop _______________
RPGN (rapidly progressive glomerulonephritis)

ESRD (end stage renal dz)
Nephritic Syndrome: IgA nephropathy (_________ disease)
Renal disease of _____ deposition in the glomerular mesangium
Cause unknown, same lesion seen in H-S purpura
Is associated with ________,__________ and ________ as in HIV and CMV
Most common form of acute GN in the US
More common in children and young adults
Males 3x more than females
Berger’s

IgA

cirrhosis, celiac dz, and infections
Nephritic Syndrome: IgA nephropathy (Berger’s Disease)
Episode of ___________ is the most common presenting complaint
Frequently associated with ____, ____ or ____ like illness
Urine is ____ or ____ colored 2 days after onset of sx
gross hematuria

URI, GI sx, or flu

red or cola
Nephritic Syndrome: IgA nephropathy (Berger’s Disease)
1/3 of patients experience clinical remission
40-50% develop progressive ____________
Remainder show _____________ but stable serum creatinine
Ominous sign is proteinuria >__g/dl
Other unfavorable indicators are HTN, ___________ microscopic hematuria and proteinuria, glomeruloschlerosis and abnormal renal functions
renal insufficiency

microscopic hematuria

1 g/dl

persistent
Nephritic Syndrome: IgA nephropathy
IgA increased up to 50% of normal, but normal IgA doesn’t r/o dz
________ is the standard for dx
_________ shows IgA granular deposits in dermal capillaries
Renal bx

skin bx
Nephritic Syndrome: IgA nephropathy
Treatment-
In significant proteinuria (>1g/dl) ______ and _______ are used to decrease proteinuria and reach target BP of 125/75
With proteinuria of 1.0-3.5 g/dl, ________ have been used and are beneficial

Other treatments-
________
Renal transplantation
But there is recurrent dz in 30% of patients 5-10 yrs post transplant
ACE-I and ARB’s

steroids

Fish oil
Nephritic Syndrome: Henoch-Schonlein purpura
Leukocytoclastic vasculitis of unknown cause

Definition: leukocytoclastic vasculitis is an acute cutaneous vasculitis that is characterized by purpura, especially of the ______, and by exudation of _________ and sometimes fibrin around dermal venules, with extravasation of ______.
Most common in ________
More in ______
legs

neutrophils

RBCs

children

males
Nephritic Syndrome: Henoch-Schonlein purpura
Clinical presentation-
Palpable purpura mostly on lower extremities
___________
GI sx such as _______, ______ and _______
Renal insufficiency with nephritic presentation
Renal lesions are identical to those in ____________
Most recover fully over several weeks
Arthralgias

nausea, colic, and melana

IgA nephropathy
Nephritic Syndrome: Pauci-immune glomerulonephritis

_______ granulomatosis, ___________ disease, and microscopic polyangitis
All are ________ vessel vasculitis
Wegners

Churg-Strauss

small
Nephritic Syndrome: Anti-glomerular Basement Membranne GN and Goodpastures syndrome

Goodpastures dz is GN and __________ hemorrhage preceded by _____ and causing hemoptysis, dyspnea and respiratory failure
______ and _______ are components of the nephritic syndrome
pulmonary

URI

HTN and edema
Nephritic Syndrome: Cryoglobulin-associated GN
Cold precipitable immunoglobulins precipitating in glomerular capillaries
Cause is underlying infection such as ________, or other occult viral, bacterial, or fungal infections
Patients have necrotizing ______ lesions in dependent areas, arthralgias, fever, and hepatosplenomegaly
Treatment is treating ____________
Hepatitis B or C

skin

underlying infection
Rapidly Progressive Glomerulonephritis:
Syndrome characterized by
___________(RBC casts and dysmorphic RBC’s)
Renal failure over weeks to months
Renal bx showing diffuse _________ formation
Can occur with or without immune deposits
Can be ___________ or superimposed on other glomerular disease
Nephronal hematuria

crescent

idiopathic
Rapidly Progressive Glomerulonephritis: Anti GBM GN
2/3 of patients have ___________ syndrome - a form of rapidly progressive glomerulonephritis, which involves a progressive decrease in the kidney's ability to function properly, accompanied by a ________ with ______ sputum.
Occurs in two peaks,
3rd to 4th decade and 6th to 7th decade
Goodpastures

cough

bloody
Rapidly Progressive Glomerulonephritis: AntiGBM GN
Goodpastures more common in the _______
Affects men more than women
Presents with RPGN, hemoptysis, and dyspnea
Strong association between ___________ and pulmonary hemorrhage in Goodpastures

Treatment-
High dose _________
_____________(Cytoxan)
High index of suspicion causing early dx and tx has increased survival to 50%. Was 10% survival 20 yrs ago
young

cigarette smoking

prednisone

Cyclophosphamide
Rapidly Progressive Glomerulonephritis: ___________ RPGN
Almost always associated with another underlying dz
Correct dx made by identifying clinical and lab features of those diseases (see table 27-4 Cecil)
Makes up 30% of all RPGN cases
(granular deposits of immunoglobulins and complement on GBM initiates glomerular injury)
Immune Complex
Rapidly Progressive Glomerulonephritis: Pauci-immune RPGN (_____ associated)
Associated with systemic vasculitides - (2)
Also an idiopathic form with vasculitis only of glomeruli
80% of Pauci-immune RPGN is associated with ANCA (antineutrophil cytoplasmic antibodies)
Treated with cytotoxic agents (______) and _________
ANCA

Wegners granulomatosis & Polyarteritis nodosa

Cytoxan and corticosteroids
Nephrotic Syndrome:

Urine _______ of >3.5g/1.73m2 per 24 hrs
Hypoalbumenemia
Hyperlipidemia
Peripheral _______
protein

edema
Nephrotic Syndrome:
1/3 of patients have systemic renal dz-
____________
Amyloidosis
SLE
HIV

Remainder have idiopathic nephrotic syndrome. 3 most common are
Minimal change disease
Focal ____________
__________ nephropathy
Diabetes mellitus

glomerular sclerosis

Membranous
Nephrotic Syndrome: Signs and Symptoms
____________ is the hallmark of the syndrome
When serum _________ concentration less than 3g/dl
But more likely due to ________ retention than low plasma oncotic pressure
Presents in the dependent areas of the body initially then becomes generalized
________ due to pulmonary edema, pleural effusions, decreased diaphragmatic excursion due to _______
Symptoms and signs of infections (more than normal) due to loss of immunoglobulins and compliment fomation
Peripheral edema

albumen

sodium

Dyspnea

ascites
Nephrotic Syndrome: Lab
___________ due to alteration in GBM
Urinary dipstick analysis indicates albumin only
Addition of sulfosalicylic acid allows other paraproteins to be detected by dipstick
Can detect as little as 15mg/dl
Must do specific gravity
Trace protein on ___________ specimen may mean nothing
Trace protein on _________ specimen may mean true renal dz
Proteinuria

concentrated

dilute
Nephrotic Syndrome: Lab - Microscopic urinalysis
Urinary sediment has few cellular elements
With significant ____________,
________ bodies - are lipid deposits in sloughed renal tubule epithelial cells
Appear as “_________” and “_______” crosses under light microscopy and polarized light
hyperlipidemia

Oval fat

grape clusters and maltese
Nephrotic Syndrome: Lab - Blood chemistries
Decreased serum _________(<3g/dl)

___________ - 50% of patients with early nephrotic syndrome
The more protein excreted, the more hyperlipidemia
Due to fall in oncotic pressure (increased protein excretion)
Decreased clearance of VLDL causing hypertriglyceridemia
Elevated ESR
albumen

Hyperlipidemia
Nephrotic Syndrome: Lab - Blood chemistries
Other tests depending on clinical presentation
________ levels
Serum ________ electrophoreisis
ANA
Serologic tests for _________
Compliment

protein

Hepatitis
Nephrotic Syndrome: Renal Biopsy
Performed in new onset idiopathic nephrotic syndrome if primary renal disorder that may require drug therapy is suspected
Not done in patients with very high _________ levels (irreversible renal dz)
Not done in amyloidosis or DM with __________ range proteinuria (irreversible renal damage)
creatinine

nephrotic
Nephrotic Syndrome: Management - Protein Loss
Daily dietary ________ intake should be increased to offset the loss and avoid negative _________ balance
Protein malnutrition occurs when urinary protein exceeds ____g/d
protein

nitrogen

10
Nephrotic Syndrome: Management - Edema
_____________ is essential
________ in most patients
Usually thiazide or loop diuretics
Both are protein bound so with hypoalbumenemia delivery to the kidney is decreased
So combination of the two can potentiate the effect
Salt restriction

Diuretics
Nephrotic Syndrome: Management - Hyperlipidemia
Dietary management of little value
But, should be advocated
_________
___________ therapy
Exercise

Pharmacologic
Nephrotic Syndrome: Management - Hypercoaguable states
Serum with low ________ (<2g/dl) can be hypercoagulable
Nephrotic syndrome patients lose antithrombin III, protein C, and protien S through the urine
Have increased _______ activation
Prone to renal vein ________
Patients with evidence of thrombus are treated with ___________ for 3-6 months
Renal vein thrombosis and recurrent thromboemboli require indefinite anticoagulation
albumen

platelet

thrombosis

anticoagulants
Nephrotic Syndrome: _______ Renal Disorders

Minimal Change Disease
Membranous Nephropathy
Focal segmental glomerular schlerosis
Primary
Nephrotic Syndrome: Primary Renal Disorders - Minimal change disease

Etiology
Mostly in _______, ______ predominence
Idiopathic or following _____ URI
Associated with _________ dz
Associated with drugs (gold and lithium)
Associated with hypersensitivity reactions especially to ________ and ______

Treatment - ________
children, Male

viral

Hodgkins

NSAIDS and bee stings

prednisone
Nephrotic Syndrome: Primary Renal Disorders - Membranous Nephropathy
Most common cause of primary nephrotic syndrome in adults
Most commonly in adults in their ______ decades
Almost always after age 30
Treatment based on renal dz progression marked by __________
Ranges from low salt diet to corticosteroids to ____________ depending on risk of progression predicted by proteinuria
5th to 6th

proteinuria

immunosupression
Nephrotic Syndrome: Primary Renal Disorders - Focal Segmental Glomerular Sclerosis
Can be idiopathic or secondary
Secondary due to morbid ______, ______ usage, and ______ infection
Typically progress to ______ in 6-8 years

Treatment
Supportive
High dose ________ can induce remission in 5-9 months in over ½ the patients
obesity

heroin

HIV

ESRD

steroids
Nephrotic Syndrome: Systemic Disorders - Amyloidosis
Extracellular deposition of a fibrous protein (amyloid) in one or more sites in the body

Serum amyloid A is synthesized in ______ and deposited in tissues in primary renal amyloidosis, may occur in absence of systemic disease or with ____________

Secondary renal amyloidosis (amyloid AA) due to chronic inflammatory dz such as RA, IBD, or chronic infection

Usually in ________ patients
________ kidneys due to amyloid deposits
liver

multiple myeloma

older

Enlarged
Nephrotic Syndrome: Systemic Disorders - Amyloidosis
Treatment and Prognosis
Treat inciting agents if present
____________
______ in 2-3 years
5 yr survival is 20%
Corticosteroids

ESRD
Nephrotic Syndrome: Systemic Disorders - Diabetic Nephropathy
*Most common cause of _______ in the US*
More common in type ___ diabetics, but increasing in type ___ diabetics
Patients at higher risk are males, African Americans, and Native Americans
Diabetic screening should always include ______________(>30mg/dl is abnormal)
In patients prone to nephropathy, microalbuminuria develops within 10-15 yrs of DM onset and progresses to overt ___________ over next 3-7 years
ESRD

1

2

microalbuminuria

proteinuria
Nephrotic Syndrome: Systemic Disorders - Diabetic Nephropathy
Strict glycemic control slows progression of nephropathy
_____ and _____ lower progression to clinical proteinuria and ESRD
____ patients also prone to papillary necrosis, chronic interstitial nephritis, and renal tubular acidosis
Poor prognosis once _________ has begun
ACE-I and ARB’s

DM

dialysis
Nephrotic Syndrome: Systemic Disorders - HIV associated Nephropathy
Can present as nephrotic syndrome in HIV patients
Mostly ________ men
More associated with ________ use
_______ slows progression of renal disease
Recommended for use in these patients
____________ treatment with cyclosporine and ACE inhibitors used with some success
young black

IV drug

HAART (highly active antiretroviral therapy)

Corticosteroid
Asymptomatic Urinary Abnormalities: Hereditary Nephritis (______ Syndrome)

Starts in childhood with microscopic hematuria with or without gross hematuria
Mild proteinuria, nephrotic syndrome rare
__________ after age 15 in 50% of patients
________ (x linked)
Boys more than girls, renal failure by age 30
No effective treatment currently available
Alports

Sensorineural deafness

Inherited
Asymptomatic Urinary Abnormalities: Thin Basement Membrane Dz
Autosomal dominant
Basement membrane glomerulopathy
Presents as _________ in otherwise healthy young adult
Excellent prognosis with only rare cases of ____________
microscopic hematuria

progressive renal failure
Asymptomatic Urinary Abnormalities: Benign Recurrent Hematuria

_______ adults with microscopic hematuria on routine exam
Gross hematuria with _________,__________,________
Young

febrile illness, exercise or immunization
Characterized by epithelial lined cavities in the kidneys filled with fluid or semi solid debris
Renal Cystic Diseases
Renal Cystic Diseases:
Clinical Settings may suggest etiology
Abdominal mass in neonate or infant suggests _______
Renal failure in an adolescent suggests ARPKD or ____________
Solitary cyst in healthy 50 year old suggests _______
A _______ history of renal disease suggests ADPKD, ARPKD, or medullary cystic disease
Recurrent __________ mostly in patients with ADPKD or medullary sponge kidney
Hematuria onset in a ________ patient indicates acquired cystic disease
ARPKD (autosomal recessive polycysitc kidney dz)

medullary cystic dz

simple cyst

family


renal stones

dialysis
Renal Cystic Diseases: Simple cyst (Solitary Cysts)
Increase in frequency with age
In up to 50% of people over age ___
Account for 65-70% of all renal masses
Found at the ________ and contain fluid which is an ultrafiltrate of plasma
Most often asymptomatic
Incidental finding during imaging study
Renal ___ and ___ differentiates benign from malignant lesions, abcess, or PKD
50

outer cortex

US and CT
Renal Cystic Disease: Simple Cysts (Solitary Cysts)
In dialysis patients, simple cysts may progress to _________
Ultrasound and CT used to differentiate

Simple cysts must have three criteria on sonogram to be considered benign:
_____ free
Sharply demarcated mass with _________
Enhanced ________(means good transmission through cyst)

_______ cysts - Thick walls, calcifications, solid components, and mixed echogenicity
malignancy

Echo

smooth walls

back wall

Complex
Renal Cystic Disease: Simple cysts (solitary cysts)

Criteria on ___-
Simple cyst
Smooth thin wall
Sharply demarcated
_______ enhance with contrast media

Renal Cell Carcinoma:
Enhances but is of lower _______ than the rest of the parenchyma

__________ can also be done pre-op
RCC is hypervascular in 80% of cases
CT

Does not

density

Arteriography
If cyst meets criteria for being benign-
Periodic _________ is the standard of care

If findings not consistent with simple cyst-
____________
evaluation

Surgical exploration
Polycystic Kidney Disease:

ADPKD
adult polycystic kidney dz

ARPKD
infantile or childhood PKD
Can occur with congenital __________ causing death from renal failure in first year of life
hepatic fibrosis
Polycystic Kidney Dz: ADPKD

Most common __________ renal dz in the U.S.
500,000 people or 1 in 800 live births
50% of patients will have ESRD by age ____
Accounts for 10% of dialysis patients in the U.S.
hereditary

60
Polycystic Kidney Dz: ADPKD
Three genes involved, two most important are ADPKD1 and ADPKD2
ADPKD 1 is on chromosome ___
ADPKD 2 is on chromosome ___
PKD 2 has slower progression and longer life expectancy than PKD 1
16

4
Polycystic Kidney Dz: Clinical manifestations

Rarely presents before age ______
So people of childbearing age pass it on before they know they have it
Patients either present for screening because of family hx, or due to symptoms
20-25
Polycystic Kidney Dz: Symptoms
Acute _________ pain and back pain with hematuria is the most common presentation
Non specific dull lumbar pain occurs when kidneys large enough to be palpable on PE
Sharp localized pain from ________,________, or calculus
_________- Frequently the initial sign of PKD, may also have gross hematuria
abdominal flank

cyst rupture, infection

Microhematuria
Polycystic Kidney Dz: S/S

_____ - Most common cardiovascular complication
In 60% of patients before the onset of renal insufficiency

______ - From urinary concentrating defect, usually present at the time of diagnosis

____,_________, and cyst infections are common complications
HTN

Nocturia

UTI, pyelonephritis
Polycystic Kidney Dz: S/S

1/3 have _______
10% have ________
25% have _____
Also, __________ associated with ADPKD
Renal function - Impairment is variable
50% of patients ESRD by age 60
hepatic cysts

cerebral anneurysms

MVP (mitral valve prolapse)

diverticulosis
Polycystic Kidney Dz: Poor prognostic indicators
ADPKD __ gene
Male
______ race
HTN
Progression at ______
Episodes of gross hematuria
1

Black

early age
Polycystic Kidney Dz: Dx
Radiographic evidence of multiple cysts in parenchyma associated with:
_______ enlargement
Increased _________ thickness
Elongation of the ________

Renal Ultrasound and CT used
CT with contrast usually shows more _______ involvement
Presence of extrarenal involvement (eg hepatic cysts) aids in dx of ADPKD
Renal

cortical

calyces

cystic
Polycystic Kidney Dz: Dx
Gene location helps identify _______________ of ADPKD1 through gene linkage analysis
Is expensive
Involves other family members
Reserved for those with ___________ imaging studies
asymptomatic carriers

nondiagnostic
Polycystic Kidney Dz: Tx of ADPKD

Preventing __________
Preserving renal function
Education regarding inheritance
Screening in patients with strong family hx of ____________
disease complications

cerebral aneurysmal hemorrhages
Polycystic Kidney Dz: Therapy
Control ____
Prevent ____
Treat cyst infections with antibiotics that penetrate cyst walls and attain therapeutic levels(3)
Dialysis or transplantation for ESRD
_________ prior to transplantation in patients with large kidneys or frequent or persistent UTI’s
HTN

UTI’s

TMP/SMX, cipro, or chloramphenicol

Nephrectomy
Polycystic Kidney Disease: ARPKD
Most common inheritable cystic renal dz occuring in ________
Is autosomal recessive, distinct from ADPKD
Involves pathologic changes in the _____ and/or kidney
Kidneys may be massively enlarged in infants
Contain multiple small subscapsular cystic spaces
infancy

liver
Polycystic Kidney Disease: ARPKD
Accounts for 1.5% of kids needing renal replacement prior to age 15
.6 % of patients with renal failure (ESRD) before the age of 20
No ______ predominance
Males ___ females
May occur at any time from perinatal period to 5 yrs old depending on classification
racial

=
Polycystic Kidney Disease: ARPKD
______ & ______ involvement
Both manifest _________ degrees of severity
If severe renal dz early, they succumb to renal dz prior to hepatic problems
But, milder forms of renal dz develop severe hepatic complications later in life
Kidney and liver

opposite
Medullary Cystic Disorders

part of a group of ______________ known as juvenile nephronophthisis-medullary cystic disease complex
Almost universal progression to _______
Childhood type (____________) is autosomal recessive
Adult type (___________) is autosomal dominant
congenital nephropathies

ESRD

Juvenile nephronopthisis

medullary cystic
Medullary Cystic Disorders: Clinical findings
Sometimes accompanied by _____________
_______ and prolonged enuresis in childhood due to concentrating defect which is early indication of renal dz
______ stature
Failure to thrive
Almost universal progression to ______
During adolescence or early adulthood
Before age 20 in juvenile form
eye deformities

Anemia

Short

ESRD
Medullary Cystic Disorders: Dx

US and CT - ___________ kidneys
Doesn’t usually show the cysts because they are only 1-2 mm in diameter

Renal biopsy - *Open renal bx* to recover tissue from ____________ junction

Treatment - No current medical therapy to prevent renal failure
______ & ______ intake to prevent renal losses
Small scarred

corticomedullary

Salt and water
Medullary Sponge Kidney

Common and benign disorder
Present at birth, not usually diagnosed until 4th or 5th decade of life
Autosomal dominant
Kidneys have very __________ enlargement in the medullary and interpapillary collecting ducts
With medullary cysts giving “________” appearance in these areas
irregular

swiss cheese
Medullary Sponge Kidney: Clinical findings
Gross or microscopic _________
Recurrent ____ or stones - may manifest itself initially as passage of renal stone
Estimated that 10% of patients who present with stones have medullary sponge kidney
Decreased urinary _________ ability
Nephrocalcinosis
Diagnosis is confirmed with ______
Accumulation of contrast in dilated collecting ducts
hematuria

UTI’s

concentrating

IVP
Medullary Sponge Kidney: Tx
No known therapy
Increasing ______ to prevent stone formation
________ diuretics to decrease calcium excretion in hypercalcuric patients
______ therapy if RTA is present
fluid

Thiazide

Alkali
Urinary Tract Obstruction

Obstruction can occur anywhere from the renal pelvis to the urethral meatus
_________ obstruction usually causes no change in flow or total renal function
If drainage of both kidneys significantly compromised, ________ or _________ can occur
Total urinary tract obstruction is an important cause of ESRD and RF
Unilateral

azotemia or renal failure
Obstruction: Clinical Presentations
Change in _________ habits frequently presenting sign
True anuria – (inability to urinate) __________ is the most common cause
Nocturia and polyuria – can result from ____________ due to defective urinary concentration
urinary

complete obstruction

partial obstruction
Obstruction
In the absence of __________, always consider obstruction as a cause of renal failure of unknown etiology
Total anuria in ____________ highly suggestive of urinary tract obstruction
proteinuria

acute renal failure
Obstruction: Diagnosis
________ is preferred means of diagnosing urinary tract obstruction
Depends on identification of __________
May not be evident in 1st 24 hrs or in severly dehydrated patient

_____ helpful in situations such as dehydration
Shows prolonged nephrogram phase with delayed filling
24 or 48 hour film may show contrast in renal pelvis or in dilated calyces
Renal US

hydronephrosis

IVP
Obstruction: Management
Identify the ________
Relieve the __________ -
Usually through surgical intervention
If cant relieve obstruction, perform urinary diversion
________ and obstruction -
Control of UTI is mandatory
UTI in obstruction is a urologic emergency and calls for prompt relief of the obstruction
site & cause

obstruction

Infection
Vascular Disorders of the Kidney: Diseases affecting the renal vasculature
Those affecting larger vessels - ________________
Ischemic nephropathy and atheroembolic disease - __________
_________ hypertension
Schleroderma
Thrombotic miroangiopathy
Renal artery occlusion

smaller vessels

Malignant
Renal Arterial Occlusion:
Potentially reversible cause of renal failure

Cause:
________ trauma or surgery
________ (heart or paradoxical thromboemboli)
Dissecting AAA or renal aneurysm
________ (polyarteritis nodosa, Kawasaki’s dz)
Renal artery _________(fibromuscular dysplasia or atherosclerosis)
External _________ of renal artery (lymph nodes, malignancy)
Abdominal

Embolism

Vasculitis

stenosis

compression
Clinical Findings of Renal Artery Occlusion:
Depend on collateral circulation
Acute renal infarct sx-
______ or _______ pain
Nausea, _______
Fever
Acute _____ due to activation of renin angiotensin system

LAB
__________, increased AST (serum aspartate aminotransferase), LDH, and alk phos.
Microscopic _________
*Renal dysfunction if bilateral/unilateral _______*
Lumbar or flank

vomiting

HTN

Leukocytosis

hematuria

infarct
Clinical findings in renal artery occlusion: Imaging
_________ imaging necessary to diagnose renal vascular occlusive disease
_________ imaging shows no blood flow to the kidney
Can use CT, MRI, or Doppler
*Renal ________ more reliably establishes diagnosis*
Radiologic

Radionuclide

Angiography
Clinical findings in renal artery occlusion: Tx
Goal is to avoid irreversible renal damage
To localize ________
To re-establish _________

Traumatic renal artery thrombosis-
Surgical __________ must be performed within 4-6 hours to prevent irreversible renal damage

Acute athroembolic disease-
Early diagnosis and prompt (HOURS) ____________- is necessary to preserve renal function
thrombus

blood flow

thrombectomy

revascularization
Clinical findings in renal artery occlusion: Chronic Ischemic Renal disease and collateral circulation
Renal function may return even if dx and tx delayed for days or weeks
Has been documented 6 weeks of return of renal function with surgical treatment up to 6 weeks after the thrombus occurred
Treatment options-
___________, IV or intra-arterial thrombolytic therapy
Percutaneous ______________, clot extraction by percutaneous catheter, surgical thrombectomy
Anticoagulation

angioplasty
Ischemic Nephropathy

Def: chronic renal impairment secondary to hemodynamically significant renal artery ________ which is a cause of renal insufficiency and ESRD
15% of ESRD patients over 50 have ________ renal disease
Prevalence of renal vascular disease is high in patients with _________,__________, or peripheral vascular disease (30-40%)
stenosis

ischemic

coronary, cerebral
Diagnosis of Ischemic nephropathy:
Must find significant ________ and show that this is the cause of renal impairment
Selection of tests depends on clinical suspicion
Example: discrepancy in ________ is good indication for considering renal artery stenosis as cause of impaired renal function
renal artery stenosis

renal size
Diagnosis of Ischemic nephropathy: Imaging

________ Ultrasonography-
Good screening test but highly operator dependent and time consuming technically difficult

_____ inhibitor renography-
Good screening test but not reliable with moderate to severe renal dysfunction

CT and MRI __________-
Effective noninvasive tests to detect renal artery stenosis
Doppler

ACE

angiography
Diagnosis of Ischemic nephropathy: Imaging
*Gold Standard for dx of ischemic nephropathy is ____________*
There are risks involved
________ induced acute renal failure - Prevent by _______, or specially prepared contrast
Atheroembolic renal disease
Irreversible loss of renal function
renal arteriography

Contrast

hydration
Recommendations for renal arteriography:
Use in patients with __________ for ischemic nephropathy
But in those with equivocal risk factors, start out with _________ tests such as Duplex Doppler US or MRA before proceeding to angiography
multiple risk factors

less invasive
Ischemic Nephropathy: Tx
________ therapy-
Doesn’t reliably prevent disease progression
But may be the only available option in those patients unable to tolerate invasive procedure

Invasive therapy-
Percutaneous __________
Surgical ___________
Both can restore renal function lost as a result of renal artery stenosis
Depends on the individual patient
Medical

angioplasty

revascularization
Ischemic Nephropathy: Tx (cont)

Percutaneous angioplasty with or without ______ is treatment of choice in high surgical risk patients

Surgical revascularization is best option in patient with high grade renal artery stenosis that is not amenable to angioplasty or in patients with renal or ______ disease
stent

aortic
Athroembolic Diseases of the Kidney:
progressive disorder with worsening renal insufficiency as a result of ___________ of small and medium sized renal vessels by atheromatous emboli

Incidence-
Occurs in patients with widespread _________ disease
Especially after renal artery manipulation or surgery
Or after angiography or percutaneous angioplasty in these patients
Can occur after treatment with __________ or ___________agents
embolic obstruction

athromatous

anticoagulants or antithrombolytic
Athroembolic Kidney Dz: Clinical concerns
Acute, subacute, or chronic renal dysfunction
Labile HTN as a result of renal _______ or activation of renin-angiotensin system
Livido reticularis – a manifestation of __________ embolization in retina, muscles, or skin (may help make the dx)
Also, cerebrovascular dz, pancreatitis, ischemic bowel, or peripheral gangrene as a result of _______ should warrant consideration of athroembolic dz of the kidney
ischemia

cholesterol

emboli
Athroembolic Kidney Dz: Tx
No effective treatment
Avoidance of ___________ or ________ procedures in patients with diffuse athroschlerosis
Avoid anticoagulants and thrombolytic agents
_________ dialysis rather than hemodalysis to avoid heparin use
Prognosis – Poor
Depends on the extent of organ involvement and the degree of embolization
angiographic or surgical

Peritoneal
Chronic Hypertensive Nephrosclerosis:
intrarenal vascular sclerosis and ischemic changes associated with chronic hypertension.
Advanced changes can lead to ESRD

Risk factors
Race (_________)
Marked elevated ________
Underlying chronic renal disease
Patients typically have long standing HTN and slowly rising serum _________
African Americans

blood pressure

creatinines
Chronic hypertensive nephrosclerosis:

dx is based on clinical presentation in long term hypertensive pt
picture is that of __________ & small kidneys on ____
usually don't need bx
degree of renal damage & progression worsened by accelerated _____
non-nephrotic proteinuria

US

HTN
Chronic Hypertensive Nephrosclerosis: Tx
Goal of therapy is to control _____
Outcome depends on BP control and patient compliance with meds, and follow up
However, renal function can worsen in some patients despite good BP control
_______ may play a part in some of these patients
BP

Genetics
________ Nephrosclerosis:
Renal vascular changes with _______ HTN causing renal ischemia and ________
Rise in arteriolar and capillary pressure causes vascular endothelium fibroid necrosis
Plasma renin-angiotensin system is activated and may contribute to this
Malignant

accelerated

acute renal failure
Malignant nephrosclerosis:
Patients present with severely elevated DBP’s (>____mm Hg)
May have hypertensive ____________
Proteinuria and hematuria with ARF
Renal bx shows fibroid necrosis of the _________
120

encephalopathy

arterioles
Malignant Nephrosclerosis: Tx
Rapidly lower the DBP to 100-110 mm Hg within __ hours
Don’t lower the mean arterial BP more than 25% for fear of ischemic events due to decreased ________
Gradual lowering of DBP to 80-90 mm Hg over weeks can then occur
Renal function decreases initially, but recovers as the lesions heal and autoregulation of blood flow occurs
Patients are at risk for coronary, cerebrovascular, and renal dz due to damage done to _________ structures
6

perfusion

vascular
Malignant nephrosclerosis:
Patients who develop renal insufficiency as a result of malignant nephrosclerosis tend to do poorly and have lower survival rate
All patients with malignant hypertension need workup of secondary causes of this problem
Malignant HTN: HTN with _________ and other organ damage such as heart failure, renal failure, and hypertensive encephalopathy
papilledema
___________:
progressive connective tissue disorder with proliferation of connective tissue, thickened vascular walls and lumen narrowing.
50% of patients have renal involvement
Mild proteinuria
Abnormal serum creatinine
Systemic hypertension
Scleroderma
Scleroderma Renal Crisis:
Occurs in 10-15% of patients
Characterized by _____
Abrupt onset of severe hypertension (small % may have normal BP)

Risk factors of renal crisis-
Rapidly progressing diffuse _____ involvement
Cooler months
__________
ARF

skin

African American
Diagnosis of scleroderma renal crisis:
Other manifestations of scleroderma
Rarely presents as the initial symptom of the disease
____, anticentromere antibody, Scl 70 antibody, and anti-RNP polymerase antibodies may be positive
ANA
Scleroderma renal crisis: Tx
Start before irreversible damage
___ control to slow renal damage progression to RF
_______ are DOC
With good BP control, patients may get enough renal function return to stop _________
BP

ACE inhibitors

dialysis
Hemolytic Uremic Syndrome and TTP:
Consist of thrombotic ___________ & ____________
Clinical features of HUS and TTP are similar
Renal involvement more in ____
______ thrombi in glomerular capillary loops
Arterioles develop fibrin thrombi with fibrinoid necrosis
microangiopathy and thrombocytopenia

HUS

Fibrin
HUS:
More in kids after non-specific _________ illness
Also, certain _______ associated with hemorrhagic colitis and HUS

HUS is associated with-
Renal failure
Thrombocytopenia
Microvascular platelet thrombi
Microangiopathic hemolytic anemia
diarrheal

E.coli
TTP-
Similar features as in HUS
But, more problems with ________ & ________ symptoms

Both disorders can be associated with-
__________
OCP’s
__________ agents
Infections
__________ diseases
mental status and neurologic

Malignancy

Antineoplastic

Autoimmune
Clinical course regarding renal involvemt in HUS or TTP can be either acute renal failure or rapidly progressive renal failure
Spontaneous recovery may be high in children who may need only __________ therapy
Adult prognosis is less favorable, may need more prolonged and additional therapy
_________ is most effective, works in 90% of cases
Should be initiated as soon as dx is made
In TTP, daily for 1 week, then alternate days until remission
__________ used in patients who don’t respond to plasma exchange
_________ for TTP patients resistant to therapy
supportive

Plasma exchange

Vincristine

Splenectomy
removing blood from the patient, mechanically separating blood from plasma, mixing blood cells with replacement plasma and returning blood mixture to the body. Purpose is to rid the blood of the immune factors that stimulates the disease process, and new plasma may dilute strenth of these immune factors
plasma exchange
Renal Vein Thrombosis:
________ in the major vein (renal vein) that drains blood from the kidney
Incidence high as 30% in _________ syndrome, especially ___________
Blood clot

nephrotic

membranous nephropathy
Acute RVT: S/S
_____
______ pain
Testicular pain
________, gross or microscopic
Marked increase in plasma ____
Rise in serum __________
Increased ______ size
N/V

Flank

Hematuria

LDH

creatinine

renal
Chronic RVT: S/S
Non specific findings
Worsening _________
Evidence of renal ________ dysfunction
_______ issues, urinary concentration, ___________ disorders
proteinuria

tubular

Acid base

electrolyte
Renal Vein Thrombosis: Dx
Gold standard is selected __________
CT, MRA, US, are useful non infasive tests, but are less reliable

Treatment-
Anticoagulation with _______ acutely, then long term anticoagulation with ________
Continue therapy for __ year or indefinitely if recurrence or risk factors
_________ therapy for acute RVT with acute renal failure
Rarely, ___________ for those who don’t respond to anticoagulant therapy
renal venography

heparin

warfarin (coumadin)

1

Thrombolytic

surgical embolectomy
Acute Renal Failure (ARF):
abrupt decrease in GFR significant enough to cause increased ______ & ______ and disruption of extracellular fluid volume and electrolyte and acid base balance

Can result from:
Diseases causing decreased renal blood flow (_________)
Diseases affecting the renal parenchyma (_________)
Diseases causing obstruction (___________)
BUN and creatinine

prerenal azotemia

azotemia

post renal azotemia
*__________ is most common intrinsic renal disease causing ARF*
ATN definition: syndrome of abrupt and sustained decline in ____ within minutes to days after ischemic or nephrotoxic occurrence
Diagnosis based on exclusion of _________, and the exclusion of other causes of intrinsic ARF:
Glomerulonephritis, acute interstitial nephritis, vasculitis
Acute tubular necrosis (ATN)

GFR

pre or postrenal azotemia
ARF: DDX
5% of hospital admissions, 30% ICU admits
H&P and lab often all that is needed for DX

In hospital:
_________ is the most common cause of azotemia
ATN is the most common problem causing ARF
So, must differentiate between them (ie from volume depletion vs insult due to nephrotoxins or ischemia)
Post renal azotemia of __________ has to be excluded in elderly males in hospital
Pre renal azotemia

bladder outlet obstruction
ARF: Diagnosis
__________
Special attention to-
Recent reduction in GFR
Events leading to deterioration of renal function
Consideration of two above factors in relation to chronology of potential causes of ARF
Must have knowledge of the natural history of different causes of ARF
Review of Records
ARF: Diagnosis - PE

Reduced body weight, postrual changes in BP and P, and decreased jugular venous pulse all suggest decreased ___________ causing prerenal azotemia

Expanded extracellular fluid volume with decreased effective blood volume-
________, nephrotic syndrome, cardiac failure

Obstruction-
__________ that indicates urinary tract obstruction
Examine prostate and do “in and out” ____________

Fever and rash with ____________
Livedo reticularis for _________ emboli
Hx of recent aortic cath suggests __________ emboli
extracellular fluid volume

Cirrhosis

Distended tender bladder

post void bladder cath

interstitial nephritis

cholesterol

atheromatous
ARF: Diagnosis - Urinalysis
Urine volume
In oliguric ATN usually ____ ml/day (but normal output does not exclude ATN as cause of ARF)
Non oliguric ATN usually associated with nephrotoxic ________-induced ARF
________ usually points to something besides ATN as cause of ARF, usually obstruction
Also, widely varying daily outputs can mean obstruction
400

antibiotic

Anuria
ARF: Diagnosis - Urinalysis
Urine sediment
Prerenal failure-increased fine _______ casts
ATN – “_______” renal tubular epithelial cells free in sediment and also in casts
Obstruction – ______ sediment
Deposition of intratubular _______ crystals as a result of methoxyflurane anesthesia in ARF
Uric acid crystal deposition seen after chemotherapy for neoplastic dz in acute hyperuricemia associated with this paraneoplastic disorder
granular

dirty brown

benign

oxylate
ARF: Diagnosis - Urinalysis
Urinary indices
Helps in determination of prerenal Azotemia vs ATN:
Urine ______
Urine ________
Urine ________
Renal failure index
Fractional excretion of filtered sodium
sodium

creatinine

osmolarity
ARF: Diagnosis - Renal ______ indications
When dx of prerenal azotemia or ATN is uncertain, especially if clinical setting suggests other possibilities (ie obstruction or vascular accident)
When clinical findings make the diagnosis of prerenal azotemia or ATN unlikely (anuria)
When oliguria persists beyond 4 weeks
biopsy
ARF: Diagnosis

Imaging
________ shows presence or absence of dilated collecting system which excludes post renal ARF (absence)
___________ assesses renal blood flow as well as excretory and secretory function

Renal bx
Useful when dx thought to be other than ________ or ________ (so may respond to disease specific treatment)
GN, vasculitis, HUS, TTP, Allergic interstitial nephritis
Ultrasound

Radionucleotide

nephrotoxic or ischemic injury
ARF: Lab
Hospitalized patients usually have _____ as cause of ARF
Outpatients, usually cause is _________- disease (once pre and post renal azotemia r/o)
Examination of the urine sediment, and blood and protein helps establish diagnosis and suggests further lab evaluation
ATN

renal parenchymal
ARF: Lab - Urine

_________ GN = 3-4+ protien, 2-3+ blood, and active urine sediment with RBC’s and casts

Myoglobinuria or hemoglobinuria = few RBC’s in urine sediment, with strongly ____+ urine seen in myoglobinuria or hemoglobinuria (myoglobinuria is prime cause of ARF in clinical “______” syndrome)

_____________= damage to muscle cells allowing contents (myoglobin) to spill into systemic circulation
Myoglobin, CPK (creatinine phosphokinase), RBC’s, pigmented casts, granular casts
Proliferative

heme

crush

Rhabodomyolysis
ARF: Diagnosis - Kidney size
*Best evaluated by ___*
Gives information as to ARF or CRF, obstruction
Ex: normal kidney size in patient with advanced azotemia means ____ rather than CRF
However, normal kidney size in patient with renal failure can also point to ___,_____, multiple myeloma, and amyloidosis
Normal kidney size in patient with kidney failure indicates need for _______ if dx not evident
US

ARF

DM, HIV

renal bx
ATN: acute renal failure due to _______ damage and accounts for 85% of intrinsic ARF

2 major causes of ATN are:
________ & _______
tubular

Ischemia & Toxin exposure
ATN: Causes - Ischemia
Caused by tubular damage from states of low ________
Characterized by inadequate GFR and inadequate renal blood flow
Inadequate blood flow cannot maintain parenchymal cellular formation
Occurs in _______ or _______ states such as dehydration, shock, and sepsis
Also in ________ involving prolonged hypoprofusion and vasodilating anesthetic agents
profusion

hypotensive or hypoxemic

major surgery
ATN: Causes - Nephrotoxic exposure

Exogenous nephrotoxins-
More commonly cause damage
________, ______, radiographic contrast agents, cysplatin, ethylene glycol, _____ inhibitors

Endogenous nephrotoxins-
_________, __________ ARF
Aminoglycosides, NSAIDS

ACE

Rhabdomyolysis, hyperuricemic
ATN: Exogenous Nephrotoxins - Aminoglycosides
25% of hospitalized patients on aminoglycosides have some degree of ATN
Nonoliguric RF _____ days after exposure
Mostly in patients with renal damage, dehydration, and advanced age
Can remain in tissues up to 1 month
Renal functions may not recover for a while after stopping
Peak and trough levels should be monitored with _______ more predictable for renal toxicity
________ & _________ are the most nephrotoxic, with ________ being the least toxic of the aminoglycosides
5-10

trough

Gentamycin and tobramycin

streptomycin
ATN: Exogenous Nephrotoxins - Other anti-infectives

_________ nephrotoxic after 2-3 grams
________, acyclovir, and several cephalosporins have associated with ATN
Amphotericin B

Vancomycin
ATN: Exogenous Nephrotoxins - Radiographic contrast agents
____ leading cause of new ARF in hospitalized patients

Predisposing factors:
Age, renal dz (serum creatinine >__mg/dl), volume depletion, diabetic nephropathy, _____, repeated dosages of contrast agents, recent exposure to NSAIDS and ACE inhibitors
Greatest risk associated with diabetes and renal dysfunction (15-50%)
3rd

2

CHF
ATN: Exogenous Nephrotoxins - Radiographic contrast agents
Toxicity usually ______ hours after contrast study

Prevention:
________ of agents recommended for high risk patients
Hydration with 1L of .45% ______ over 12 hours before and after procedure
___________ 600mg Q12h before and after dye administration in patients with lower GFR may be beneficial (unknown MOA)
24-48

Lower volumes

saline

Acetylcysteine
ATN: Exogenous nephrotoxins - Cyclosporin
Dose dependent
Distal tubular dysfunction from severe ___________
Monitoring is important to prevent toxicity
In renal transplant patients taking cyclosporin to prevent rejection, ________ is necessary to determine if RF is due to transplant rejection or cyclosporin toxicity
Renal function improves after stopping drug
vasoconstriction

renal bx
ATN: Exogenous Nephrotoxins - Others

Antineoplastics: _________

Organic solvents, ethylene glycol

Heavy metals: ________, cadmium, and arsenic
Cysplatin

Mercury
ATN: Endogenous Nephrotoxins - Heme containing products
________ as a result rhabdomyolosis leads to ATN
Necrotic or damaged muscles release myoglobin
Large amounts of myoglobin are filtered across glomerulus
Myoglobin is resorbed by renal tubules causing damage
Obstruction of tubules by _______ casts, and intrarenal __________ also causes damage
Myoglobinuria

pigmented

vasoconstriction
ATN: Endogenous nephrotoxins - Heme containing products
Rhabdomyolosis causes of renal failure
__________
____________ from prolonged unconsciousness
Seizures
Cocaine
________ abuse
__________ and acidosis predispose to myoglobinuric renal failure
Crush injury

Muscle necrosis

Alcohol

Dehydration
ATN: Endogenous Nephrotoxins - Rhabdomyolosis and renal failure
Clinical and lab findings
Muscle ______, muscle ______
____ levels of 16,000-50,000 signals Rhabdomyolosis of clinical importance
Urine dipstick will be falsely ___ for hemoglobin due to globin portion of myoglobin
Urine is ________ with NO RBC’s
_______– hyperkalemia, hyperphosphatemia, and hyperuricemia
pain

injury

CK

+

dark brown

Blood
ATN: Endogenous Nephrotoxins

Rhabdomyolysis and renal failure - Treatment
_________ is the most important thing
________ for diuresis and alkalinization of the urine

Other Endogenous Nephrotoxins
_______ in massive intravascular hemolysis such as transfusion reactions and hemolytic anemias
Hydration

Mannitol

Hemoglobin
ATN: Other Endogenous Nephrotoxins
________ in rapid cell turnover and lysis
Caused mostly by ____________ for germ cell neoplasms and leukemias
ARF occurs with deposition of uric acid crystals in the tubules
Uric acid levels >____
Urine uric acid > 600mg/24hrs
Urine uric acid to urine creatinine ratio of >__ indicates strong risk for ARF
Hyperuricemia

chemotherapy

20

1
ATN: Lab
Sediment shows pigmented granular “_______” casts
_________ epithelial cells and epithelial cells present
Hyper______
hyper________
muddy brown

Renal tubular

hyperkalemia

hyperphosphatemia
ATN: Treatment
Preventative measures to avoid hyperkalemia and volume overload
______ diuretics have been used for adequate diuresis and may help convert oliguric to nonoliguric renal failure
But widespread use in critically ill patients with _____ should be avoided
Nutritional support to prevent excessive catabolism
________ restriction to prevent metabolic acidosis
Hypocalcemia and hyperphosphatemia treated with diet and phosphate binding agents
Avoidance of ________ containing acids due to hypermagnesemia
Loop

ARF

Protein

magnesium
ATN: Treatment - Dialysis indications
Life threatening ________ disturbances such as hyperkalemia
Volume overload unresponsive to ________
Worsening _______ or uremia (encephalopathy, pericarditis, seizures)
In gravely ill patients, less severe but worsening problems may indicate dialysis
electrolyte

diuretics

acidosis
ATN: Prognosis - Mortality
20-50% in medical illness, 70% in surgical setting
Increased mortality associated with advanced age, severe underlying disease, and multisystem organ failure
Leading causes of death are _________, ________ & ________ disturbances, and worsening underlying disease
Mortality rates haven’t changed in the last 20 years
_________ is a high priority
infections

fluid and electrolyte

Prevention
ARF: Other Endogenous Nephrotoxins - Hepatorenal syndrome
Kidney failure in patients with severely compromised _______ functions
No other clinical, laboratory, or anatomic reasons for renal failure
In U.S., mostly advanced __________

Precipitating causes:
Deteriorating liver functions, sepsis, nephrotoxic _______ or _______ usage, overuse of diuretics, diarrhea, or GI _______
May have no precipitating cause
liver

alcoholic cirrhosis

antibiotic or NSAID

bleed
ARF: Endogenous Nephrotoxins

Hepatorenal syndrome:
HALLMARK is ________ with urinosmolality 2-3 times the concentration of plasma, in urine that is almost completely ________ free as in patients with _________ azotemia
oliguria

sodium

prerenal
Endogenous Nephrotoxins: ARF related to pregnancy -
Rare in industrialized nations
Decrease thought due to legalization of _________ in many countries
Associated with _______ following an abortion
Most common infection associated with ARF of pregnancy is ________
Clinical picture is _________ as a result of toxin production, hypotension, hemorrhage, sepsis, and DIC
abortion

infection

Clostridium

hemolysis
ARF: Endogenous Nephrotoxins - ARF of Pregnancy
___________ is one of the most common medical complications of pregnancy
25% of the patients develop a transient decline in GFR
Treat with ____ antibiotics with follow up oral antibiotic therapy for ___ weeks
_____ trimester - ARF associated with pre-eclampsia, post partum hemorrhage, amniotic fluid embolism, placental abruption, and retained fetal placental parts
Pyelonephritis

IV

2

Third
ARF: Interstitial Nephritis
10-15% of causes of RF
Pathology – interstitial inflammatory response with _______ and tubular cell damage
_______ account for over 70% of cases
Can occur in infectious diseases, immunologic or idiopathic conditions
edema

Drugs
ARF: Interstitial Nephritis
Most common causative drugs are-
__________
__________
Sulphonamides and sulphonamide containing ________
NSAIDS
Rifampin
________
Allopurinol
Penicillins

Cephalasporins

diuretics

Phenytoin
ARF: Interstitial Nephritis

__________-
Streptococcal infection
Leptospirosis
CMV
Histoplasmosis
Rocky mountain spotted fever

____________-
SLE
Sjorgrens
Sarcoidosis
Cryoglobulinemia
Infections

Immune disorders
ARF: Interstitial Nephritis - Clinical Findings
_______
_______
________
Eosinophilia in peripheral blood
______ contains red cells, white cell, and WBC casts
Proteinuria
eosinophyluria
Fever

Rash

Arthralgias

Urine
ARF: Interstitial Nephritis - Treatment
Good prognosis with recovery usually in weeks to months
________ may be necessary acutely
Very rarely progress to _____
Worse prognosis is oliguric RF and ________
Treatment is supportive and removal of offending agent
Short course of _______ if renal failure persists
Dialysis

ESRD

advanced age

steroids
progressive and irreversible loss of renal function
Chronic Renal Failure (CRF)
CRF: Watching lab is important
Can have up to 75% loss of GFR without ________ due to adaptation of remaining glomeruli and tubules
But, rise in serum _________ from .7 to 1.4 signifies 50% loss of GFR
Early intervention is important at this stage
So, serum creatinine and creatinine clearance is used for diagnosis and monitoring renal dysfunction
symptoms

creatinine
CRF: CRF vs ARF
Past and present serum creatinine measurements
Search for causes of CRF
_________ for definitive dx
Allows for:
Diagnosis and treatment
Prognosis
Determination of need and suitability for _________
Renal bx

renal transplant
CRF: CRF vs ARF
If no bx
Dx based on
Past, present, and family _______
Serology
Examination of urine _______
Renal _______

Kidney size-
Most CRF associated with ________ kidney size
Some have normal kidney size even with advanced failure
DM, Multiple Myeloma, polycystic kidney dz, HIV nephropathy, amyloidosis
history

sediment

ultrasound

decrease
CRF: Conservative management of CRF

Slow ________
Control HTN, diabetes, and hyperlipidemia,
Avoid nephrotoxins
_______ cessation
Block production or effect of angiotensin ____

Identify reversible causes when renal functions decline unexpectedly
Identify and treat complications of CRF
Prepare patients emotionally and physically for ESRD and renal replacement therapy (RRT)
progression

Smoking

II
CRF: Managing ____
Slows the rate of renal failure, especially in patients with diabetic nephropathy
Nephroprotective effect of meds that block the production and/or effect of angiotensin II in patients with type 1 and 2 diabetic nephropathy
____(nonhydropyridines) also slow the progression of renal disease (verapamil, diltiazem)
Will need an average of 2.7 antihypertensive medications to reach optimal BP in patients with significant proteinuria and diabetes
HTN

CCB’s
CRF: Managing Diet

Dietary _______ restriction slows the rate of progression of renal insufficiency

Also advocated to reduce features of _______ syndrome
protein

uremic
CRF: Managing Diet
National Kidney Foundation Practice Guidelines for Nutrition in CRF of patient with GFR of less than 25 ml/min or patients on RRT
35Kcal/day under 60 yrs old
30 Kcal/day for those over 60 yrs old
0.6 - 0.75g/kg/day of protein, with 50% being of high biologic value
______ restriction in hypertensive and edematous patients
__________ at the outset of dialysis has higher mortality rate
So protein restriction should be approached with caution with assurance of adequate _______ intake
Sodium

Malnutrition

calorie
CRF: Management of reversible causes of acute deterioration of renal function

Can plot out the rate over time at which a specific patient will reach _____
If the patient shows sudden deterioration in renal disease, look for reversible cause
Patients with CRF are more susceptible to those factors causing ____
ESRD

ARF
CRF: Avoiding Toxic Drug effects

Avoid __________- Most common offender in hospitalized patients

Avoid ________ - Inhibits vasodilitory prostaglandins and decreases GFR; Also causes interstitial nephritis and ARF

Avoid ________ agents- High risk patients are those that are volume depleted and those with preexisting renal insufficiency
Increase fluid hydration with D5 ½ NS 8-10 hours before and after procedure
________(dopamine receptor agonist) which causes renal and systemic vasodilation may prevent contrast nephropathy in high risk patients
aminoglycosides

NSAIDS

radiocontrast

Fenoldopam
CRF: General Features of Uremic Syndrome - Clinical Manifestations

Uremia def: an excess in the blood or urea, creatinine, and other nitrogenous end products of _______ & ________ metabolism. Also known as _______

Uremic Syndrome effects every organ system
Due to retained molecules, ______ deficiencies, metabolic factors
protein and amino acid

Azotemia

Hormone
CRF: Clinical Manifestations ______ causes fatigue, nausea, vomiting, and headaches

_______ (product of urea breakdown) can cause carbamylation of lipoproteins and peptides resulting in multiple organ dysfunction

_______ (biproducts of protein metabolism) are increased in renal failure
Inhibit alpha 1 hyroxylase in kidney leading to deficient calcitriol production causing secondary hyperparathyroidism
High levels of parathyroid hormones implicated in ________ in uremia
Urea

Cyanate

Guanidines

cardiomyopathy
Cardiovascular
Gastrointestinal
Neurologic
Musculoskeletal
Hematologic
Endocrine
Immunologic
Metabolic
Dermatologic
Specific Manifestations of Uremic Syndrome
CRF: Cardiovascular Effects
Death from ____ in CRF is 3 ½ times greater than age matched population
Heart dz accounts for 50% of the deaths of uremic patients
60% of patients have ___ on echo with dilation, systolic, and diastolic dysfunction
______ and HTN contribute to LVH and CHF
CVD

CHF

Anemia
CRF: Cardiovascular Effects (cont)
2° hyperparathyroidism causes metastatic _________ in myocardium, heart valves, and arteries
_________ is accelerated with high rate of recurrence post angioplasty
_______ before and during dialysis due to inadequate dialysis
Resolves with dialysis intensification
If it doesn’t surgical drainage or _______ are used
calcification

Athrogenesis

Pericarditis

NSAIDS
CRF: Gastrointestinal Disease
GI disturbances are among the earliest and most common signs of the uremic syndrome
______ taste and ________ early on
Later, anorexia continues, nausea, vomiting, and weight loss (improves with dialysis)
______ from gastritis, ulcers, and arteriovenous malformations
Metallic

anorexia

GI bleeds
CRF: Neurologic Manifestations
CNS manifestations are frequent and occur early
Subtle changes in cognitive functions and ______
_______ disturbances
Lethargy, irritability, frank encephalopathy, asterixis, and seizures are late manifestations
Bilateral __________ neuropathy
Restless leg, footdrop, wristdrop
PE: decreased _______ and loss of ________ sense
memory

Sleep

glove and stocking

DTR’s

vibratory
CRF: Musculoskeletal manifestations
Alterations in calcium and phosphate homeostasis
Hyperparathyroidism and disturbances of Vit ___ metabolism
Hypocalcemia and hyperparathyroidism cause ______ retention and lack of alpha 1 hydroxylase activity in the failing kidney, with deficiency of Vit D (_______) as the consequence
In time adaptive hyperparathyroidism becomes maladaptive, and this leads to bone disease and tissue calcinosis (___________)
Can be controlled with dietary phosphate restriction, phosphate binders, calcium supplements, Vit D and Vit D analogs, and dialysis
D

phosphate

calcitriol

renal osteodystrophy
CRF: Hematologic Effects

____(regulates erythrocyte production) decreases as renal mass decreases
____ and EPO deficiency are common causes of anemia in CRF
EPO administration improves quality of life, corrects anemia, and decreases need for blood transfusions

Bleeding disorders-
Due to defects in platelet aggregation and adherence
Controlled with _______, _________, conjugated ________, and dialysis
EPO

Iron

vasopressin, cryoprecipitate, conjugated estrogens
CRF: Endocrine Abnormalities
Alterations in _______ function
Increased T3 resin uptake (low TBG levels)
Low T3 due to impaired conversion of ______ to T3 in the periphery
Normal TSH and throxine (T4)
_______ is present in 1/3 of patients with CRF
thyroid

thyroxine

Goiter
CRF: Endocrine Abnormalities (cont)
Abnormal _________ axis
________ dysfunction manifested by impotence, decreased libido, amenorrhea, sterility, and uterine bleeding
Hypoprolactinemia
Decreased estrogen, testosterone, and progesterone with normal ____ & ____
_______ uncommon in female patients with GFR less than 30 mL/min
pituatary-gonadal

Sexual

FSH and LH

Pregnancy
CRF: Immunologic Function
Defects in _______ & _______ immune systems in patients with end stage renal disease

Patients susceptible infections:
Bacterial
_______
Microbacterial
humoral and cellular

Fungal
CRF: Metabolic Disorders

Decreased renal function means decreased _______ requirement

Due to increased half life of exogenous insulin because of decreased insulin clearance
Increased insulin ______ due to tissue insensitivity, metabolic _____ , and hyperparathyroidism which impair insulin release and secretion
insulin

resistance

acidosis
CRF: Metabolic disorders (cont)
______ abnormalities consistant with type IV hyperlipidemia
Marked increase in TG, less of an increase in cholesterol
Due to decreased lipoprotein lipase in uremia
Decreases the conversion of VLDL to LDL
Results in ___________
These abnormalities result in accelerated ________ and _________ proliferation with progressive renal failure
Lipids

hypertriglyceridemia

atherosclerosis and mesangial cell
CRF: Dermatologic Manifestations

Uremic ___ from retained liposoluable pigments

_______ is common
Responds to dialysis, control of hyperparathyroidism, balance of calcium and phosphate, UV rays

Nail findings
________ nail
Red, pink, or brownish discoloration of the ______ nail bed
Pale nails
__________
Hue

pruritis

Half and half

distal

Splinter hemorrhages
Hemodialysis

Peritoneal Dialysis

Kidney Transplantation
Treatment of End Stage Renal Failure (ESRD)
Treatment of ESRD:
Treatment plan should be in place ______ in the course of renal failure before uremic symptoms appear

Criteria for the initiation of dialysis:
GFR ___ ml/min or less in diabetic patients
GFR ___ ml/min or less in those without diabetes
Start above these ranges in patients with-
Volume overload resistant to diuretics
Metabolic acidosis
Pericarditis
Persistant hyperkalemia
Intractable GI sx, or encephalopathy
early

15

10
Treatment of ESRD:
Choice of renal replacement therapy depends on patient’s physical or sociodemographic characteristics
Patients may be started on _________ or _________
____________ encouraged because it allows for better quality of life and chance for rehabilitation
hemodialysis or peritoneal dialysis

Renal transplantation
Treatment of ESRD: ________
The most common modality for RRT in the US

Average patient requires 4 hours dialysis 3 times weekly to remove toxins
Hemodialysis
Treatment of ESRD: Peritoneal Dialysis
The trend in the US is to move more patients toward peritoneal dialysis

Advantages
Patients do not have to spend hours in dialysis unit
No stringent _______ restrictions as in hemodialysis
_____ rates are better than in hemodialysis, with more patients returning to full employment
Residual renal function is maintained _______ while patient undergoing peritoneal dialysis, reducing morbidity and mortality
dietary

Rehab

longer
Treatment of ESRD: Peritoneal Dialysis

Method
The ________ acts as a semipermeable membrane similar to a hemodialysis filter

2-3 liters of _______ instilled into the peritoneal cavity for varying amounts of time
Exchanged ____ times daily
peritoneum

dialysate

4-6
Treatment of ESRD: Peritoneal Dialysis

Method - __________ peritoneal dialysis
Patient is connected to machine called a cycler
Allows inflow of smaller volumes of dialysate with shorter dwell time through the night while patient sleeping
Continuous cyclic
Treatment of ESRD: Peritoneal dialysis

Rate of removal of solutes depends on:
_______ gradient, surface area, and permeability of the peritoneal membrane to the solute
_______ molecules move easily and are influenced by the ultrafiltration rates
Ultrafiltration enhanced by increasing _______ in the dialysate
Concentration

Smaller

dextrose
Treatment of ESRD: Drawbacks of peritoneal dialysis

________ of the percutaneous catheter placed in peritoneum
_________ treated with intraperitoneal antibiotics
________ removed in bacterial peritonitis not responding to antibiotics and in fungal peritonitis

Difficulty in achchieving adequate clearance in patients with ________
Infection

Peritonitis

Catheter

large body mass
Treatment of ESRD: Kidney Transplantation
The preferred modality of RRT

______________ often required before, during, or after transplantation
_________ marked significant improvement in success rate of renal transplantation
From 65% graft survival in 1983 to 90% today
Further decrease in rejection seen with newer ____________ agents
Also, increase in short term allograft survival due to these agents with 1 year graft survival in cadaveric transplants up to 90%
Hemo or peritoneal dialysis

Cyclosporine

immunosupressive
Treatment of ESRD: Immunosupressant drug therapy
Prophylaxis and treatment of graft rejection are at the heart of the success of kidney transplantation
Protocals aimed at disruption of _______ cell cycle
Different agents have specific MOA
_________ system is essential for some ot the agents to work and changes in their levels can be due to patients taking one of several drugs that can induce or inhibit the system
Major drugs are ________, _________, _________, ________
lymphocyte

Cytochrome P-450

Cyclosporin, tacrolimus, mycophenolate, Rapamycin
Treatment of ESRD: Kidney Transplantation - Acute Rejection

Clinically detected by:
Graft ________
Rise in serum _______
Oliguria
Resulting tubulitis
_______

Frequent monitoring of renal function allows early detection of increased creatinine (acute rejection) prior to _________ appearing

Acute rejection episodes (< __ days) have a negative impact on long term graft survival
tenderness

creatinine

fever

clinical symptoms

60
Treatment of ESRD: ____________

2nd only to vascular dz as leading cause of mortality in post transplant patients
Community acquired bacterial and viral infections
Viral, fungal, and other opportunistic infections which normally don’t cause severe illness in immunocompetent hosts

Timetable is predictable
Educated guess based on time after transplantation and symptoms associated with each infection helps facilitate early recognition and treatment pending confirmatory tests
Post Transplant Infection
Treatment of ESRD: Post-Transplant Malignant Disease

Immunosuppression increases risk of ________
________ (mostly squamous cell) has highest incidence in transplant recipients
Caution regarding sun exposure
Skin protection for primary prevention

High risk also for _______ lymphoma, ______ sarcoma, and post transplant lymphoproliferative disease (rare in immunocompetent host)
malignancy

Skin cancer

non-Hodgkins

Kaposi’s
Treatment of ESRD: Malignancies

_________ is important part of post transplant follow up

Patient education to report the following:
Early changes in _____ habits
_______ symptoms
Hematuria
Skin changes
______ changes
Musculoskeletal symptoms
Cancer surveillance

bowel

Respiratory

Weight
Nephritic Syndrome S/S

PHAROH
Proteinuria, Hematuria, Azotemia, RBC casts, Oliguria, Hypertension
Nephrotic syndrome: causes for secondary nephrotic syndrome

DAVID
Diabetes mellitus
Amyloidosis
Vasculitis
Infections
Drugs
Renal failure: symptoms/signs

My Big Nob Vibrates Gently In Her Purulent Pelvis
Malaise
Breathlessness
Nausea
Vomiting
GI motility
Headache
Pruritis
Pigmentation