Altered Renal Altered Renal FunctionFunction

Overview of Kidney Overview of Kidney DiseasesDiseases

Classified by site or cause of diseaseClassified by site or cause of disease Organization by site:Organization by site:

– PrerenalPrerenal– Intrarenal (Renal)Intrarenal (Renal)– PostrenalPostrenal

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Prerenal diseasePrerenal disease Results from inadequate blood flow to Results from inadequate blood flow to

the kidneythe kidney– Decreased intravascular volumeDecreased intravascular volume– Lesions in the renal arteriesLesions in the renal arteries– Hypotension Hypotension

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Renal diseasesRenal diseases

Result from direct damage to Result from direct damage to nephronnephron

Glomerular disordersGlomerular disorders Tubulointerstitial disorders – Tubulointerstitial disorders –

disorders of the medullary tubules disorders of the medullary tubules and interstitial cellsand interstitial cells

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Postrenal diseasesPostrenal diseases

Commonly due to urinary tract Commonly due to urinary tract obstructionobstruction– Kidney stonesKidney stones– Tumors of bladder, ureters or Tumors of bladder, ureters or

prostate glandprostate gland

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Obstructive DisordersObstructive Disorders

Interference with urine flow at any Interference with urine flow at any pointpoint

Anatomic or functionalAnatomic or functional Impedes flow proximal to blockageImpedes flow proximal to blockage Dilates urinary systemDilates urinary system Increases risk for infectionIncreases risk for infection Compromises renal functionCompromises renal function Anatomic changes are called Anatomic changes are called

obstructive uropathyobstructive uropathy66

Causes of obstructionCauses of obstruction Congenital malformationsCongenital malformations Stones Stones Abdominal tumor or inflammation Abdominal tumor or inflammation

and scarringand scarring Tumor of urinary system or prostateTumor of urinary system or prostate Severe pelvic organ prolapse in Severe pelvic organ prolapse in

womenwomen

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Consequences depend Consequences depend on:on: Location of lesionLocation of lesion Whether one or both upper urinary Whether one or both upper urinary

tracts are involvedtracts are involved Severity and completeness of Severity and completeness of

blockageblockage Duration of blockageDuration of blockage Nature of the lesionNature of the lesion

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Obstruction causes Obstruction causes dilation:dilation:

Of ureters – hydroureterOf ureters – hydroureter Of renal pelvis and calyces –Of renal pelvis and calyces –

hydronephrosishydronephrosis Of both - ureterohydronephrosisOf both - ureterohydronephrosis

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There was a large renal calculus (stone) that obstructed the calyces of the lower pole of this kidney, leading to a focal hydronephrosis (dilation of the collecting system).

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Here is a kidney with much more advanced hydronephrosis in which there is only a thin rim of remaining renal cortex

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Initial tubular damage decreases the Initial tubular damage decreases the ability to concentrate urine, causing ability to concentrate urine, causing an increase in urine volume, an increase in urine volume, decrease concentrationdecrease concentration

Affected kidney cannot conserve Affected kidney cannot conserve water, sodium, or bicarb, or excrete water, sodium, or bicarb, or excrete potassium, or hydrogen ions.potassium, or hydrogen ions.

Leads to metabolic acidosis and Leads to metabolic acidosis and dehydration.dehydration.

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Recovery depends on Completeness of Recovery depends on Completeness of blockage and duration.blockage and duration.

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Body can partially compensate if one Body can partially compensate if one kidney is affected by compensatory kidney is affected by compensatory hypertrophy of other kidneyhypertrophy of other kidney– No increase in number of nephronsNo increase in number of nephrons– Increase in size of glomerulus and Increase in size of glomerulus and

tubulestubules– Ability decreases with ageAbility decreases with age– Is reversible if other kidney Is reversible if other kidney

recoversrecovers

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Relief of obstruction of partial Relief of obstruction of partial obstruction of both kidneysobstruction of both kidneys

Usually mildUsually mild Restores fluid and electrolyte balanceRestores fluid and electrolyte balance Occasionally, can result in output of Occasionally, can result in output of

10L/day10L/day Can cause dehydration and electrolyte Can cause dehydration and electrolyte

imbalanceimbalance

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Obstruction of bladder outlet or Obstruction of bladder outlet or urethra affects upper and lower urethra affects upper and lower

tractstracts.. Partial obstruction can lead to over active bladder and Partial obstruction can lead to over active bladder and

urine retentionurine retention Can back up and cause hydroureter, hydronephrosis Can back up and cause hydroureter, hydronephrosis

and impaired kidney functionand impaired kidney function Urine can be a microbiological growth medium – Urine can be a microbiological growth medium –

infection of obstructed kidney can cause further infection of obstructed kidney can cause further damage and scarringdamage and scarring

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Could lead to HypertensionCould lead to Hypertension

Renin-angiotensin pathway in Renin-angiotensin pathway in acute unilateral obstructionacute unilateral obstruction– Increased renin Increased renin angiotensin I angiotensin I

angiotensin II angiotensin II increased increased aldosterone aldosterone increased Na and increased Na and water retentionwater retention

Due to water and sodium and urea Due to water and sodium and urea retention in chronic bilateral partial retention in chronic bilateral partial obstructionobstruction

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Kidney stones or renal Kidney stones or renal calculicalculi Masses of crystals, protein or Masses of crystals, protein or

other substancesother substances Common cause of obstruction in Common cause of obstruction in

adultsadults 2-3 % of U.S. population2-3 % of U.S. population Recurrence within 10 years is 50 Recurrence within 10 years is 50

%%

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Influenced by age, gender, race, Influenced by age, gender, race, geographic location, season, fluid geographic location, season, fluid intake, diet and occupation. intake, diet and occupation.

Seen in more men than womenSeen in more men than women Less risk if physically active and Less risk if physically active and

drink adequate waterdrink adequate water Other risk factorsOther risk factors

– Overweight, Caucasian, previous stones, Overweight, Caucasian, previous stones, infectionsinfections

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Type of Stone Frequency

Calcium oxalate (or phosphate) 75% - more in men

Magnesium ammonium phosphate 12% (struvite, or "triple phosphate")

- more in womenUric acid (Gout) 6%

Cystine 1%

Other 6%

Increased renal excretion of these Increased renal excretion of these moleculesmolecules

Decreased urine volumeDecreased urine volume Change in pH of urineChange in pH of urine

– Alkaline urine increases risk of calcium Alkaline urine increases risk of calcium phosphate stonesphosphate stones

– Acid urine increases risk of uric acid Acid urine increases risk of uric acid stonesstones

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Size of stone determines Size of stone determines likelihood it will be likelihood it will be passed.passed. < 0.5 cm 50 % chance< 0.5 cm 50 % chance 1 cm almost no chance ( unless 1 cm almost no chance ( unless

ureter dilated by previous ureter dilated by previous passage)passage)

Develop in renal tubules, calyces, Develop in renal tubules, calyces, ureter or bladderureter or bladder

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Clinical manifestationsClinical manifestations

Pain (renal colic) – can determine Pain (renal colic) – can determine locationlocation

Nausea / vomitingNausea / vomiting Chills, feverChills, fever hematuriahematuria

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TreatmentTreatment

Urinalysis and analysis of stonesUrinalysis and analysis of stones Removal by surgery/ Removal by surgery/

percutaneous lithotripsypercutaneous lithotripsy Drugs to dissolve stonesDrugs to dissolve stones

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Prevention of future Prevention of future stonesstones Treat underlying metabolic disordersTreat underlying metabolic disorders Water intake = urine output of 2 -3 L /dayWater intake = urine output of 2 -3 L /day Reduction in dietary oxalates (chocolate, Reduction in dietary oxalates (chocolate,

nuts, soybeans, rhubarb and spinach) and nuts, soybeans, rhubarb and spinach) and animal protein for uric acid stonesanimal protein for uric acid stones

Increased dietary fiberIncreased dietary fiber Do Do NOTNOT decrease calcium intake – increases decrease calcium intake – increases

risk of stonesrisk of stones

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Urinary Tract Urinary Tract infectionsinfections Bacteria most common causeBacteria most common cause Can also be due to viruses, fungi Can also be due to viruses, fungi

or parasitesor parasites Classified by location in system or Classified by location in system or

by complicating factorsby complicating factors

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Cystitis – inflammation of the bladderCystitis – inflammation of the bladder– Urinary frequencyUrinary frequency– Dysuria – painful or difficult urinationDysuria – painful or difficult urination– UrgencyUrgency– Lower abdominal, lower back or Lower abdominal, lower back or

suprapubic painsuprapubic pain May be uncomplicated in otherwise May be uncomplicated in otherwise

healthy individualhealthy individual

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IncidenceIncidence Young adult women – 0.2/monthYoung adult women – 0.2/month Lifetime risk in women 50%Lifetime risk in women 50% Young adult men prevalence < 1%Young adult men prevalence < 1% High risk groups:High risk groups:

– Premature infantsPremature infants– Sexually active womenSexually active women– Women using a diaphragm or Women using a diaphragm or

spermicidespermicide– DiabeticsDiabetics– HIV or immunosuppressive disordersHIV or immunosuppressive disorders– Obstruction of lower urinary tractObstruction of lower urinary tract 3030

Most UTIs are caused by:Most UTIs are caused by:

gram negative bacteria of the intestinal gram negative bacteria of the intestinal tracttract

Escherichia coliEscherichia coli – 80% of all uncomplicated – 80% of all uncomplicated infections. Can form pili allowing infections. Can form pili allowing bacterium to adhere to bladder epitheliumbacterium to adhere to bladder epithelium

Cranberry juice decreases bacterial Cranberry juice decreases bacterial adhesions by epicatechinadhesions by epicatechin

Staphylococcus saprophyticusStaphylococcus saprophyticus 10-20% 10-20%

Other entreobacter species (Other entreobacter species (Klebsiella, Klebsiella, ProteusProteus) remaining 5%) remaining 5%

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TreatmentTreatment

AntibioticsAntibiotics Drink normal amounts of water, Drink normal amounts of water,

but avoid bladder irritants, such but avoid bladder irritants, such as caffeineas caffeine

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Nonbacterial cystitisNonbacterial cystitis Same symptoms but without Same symptoms but without

infectioninfection Dysfunction of external sphincter, Dysfunction of external sphincter,

urethritis, or inflammation of glands urethritis, or inflammation of glands near vaginanear vagina– antibiotics, drugs to relax urethral antibiotics, drugs to relax urethral

sphincter, retraining of voiding habitssphincter, retraining of voiding habits Interstitial cystitis – may be due to an Interstitial cystitis – may be due to an

autoimmune reaction, mucus autoimmune reaction, mucus deficiency or abnormal mast cells.deficiency or abnormal mast cells.

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Tubulointerstitial Tubulointerstitial disordersdisorders Acute pyelonephritis (pyelo – pelvis)Acute pyelonephritis (pyelo – pelvis)

– Urinary obstruction and reflux of urine Urinary obstruction and reflux of urine most common risk factorsmost common risk factors

– One or both kidneys may be involvedOne or both kidneys may be involved– Most common in womenMost common in women– Usually Usually E. coli, ProteusE. coli, Proteus or or PseudomonasPseudomonas– Usually By ascending microorganisms, Usually By ascending microorganisms,

but can be carried in blood.but can be carried in blood.

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Acute pyelonephritisAcute pyelonephritis

Inflammation is usually focal, Inflammation is usually focal, affecting pelvis, calyces, and medulla affecting pelvis, calyces, and medulla but glomeruli not usually involved.but glomeruli not usually involved.

Kidney is infiltrated with wbc’s – Kidney is infiltrated with wbc’s – pyuriapyuria

Healing involves scarring and Healing involves scarring and atrophy of affected tubulesatrophy of affected tubules

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Acute pyelonephritisAcute pyelonephritis Clinical manifestations:Clinical manifestations:

– Acute onsetAcute onset– Fever or chillsFever or chills– Flank or groin painFlank or groin pain– Frequency and dysuriaFrequency and dysuria

May be difficult to distinguish from May be difficult to distinguish from cystitis – look for white cell castscystitis – look for white cell casts

Treatment:Treatment:– Microorganism specific antibioticsMicroorganism specific antibiotics

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Chronic PyelonephritisChronic Pyelonephritis Cause is more difficult to determineCause is more difficult to determine More likely in patients with reflux or renal More likely in patients with reflux or renal

stonesstones Scarring can lead to impaired urine-Scarring can lead to impaired urine-

concentrating ability, leading to chronic concentrating ability, leading to chronic renal failurerenal failure

May be due to drug toxicity from analgesics, May be due to drug toxicity from analgesics, such as phenacetin, aspirin, acetaminophensuch as phenacetin, aspirin, acetaminophen

Ischemia, radiation, immune-complex Ischemia, radiation, immune-complex diseasedisease

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Chronic PyelonephritisChronic Pyelonephritis

Manifestations are often minimal- Manifestations are often minimal- – HypertensionHypertension– Frequency and DysuriaFrequency and Dysuria– Flank painFlank pain

Diagnosis Diagnosis – UrinalysisUrinalysis– Intravenous pyelography, ultrasoundIntravenous pyelography, ultrasound

TreatmentTreatment– Relieve obstructionRelieve obstruction– antibioticsantibiotics

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Normal glomerulusNormal glomerulus

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Acute pyelonephritisAcute pyelonephritis

4141At high magnification, many neutrophils are seen in the tubules and interstitium in a case of acute pyelonephritis.

Ascending bacterial infectionAscending bacterial infection

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This is an ascending bacterial infection leading to acute pyelonephritis.

Chronic pyelonephritisChronic pyelonephritis

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Chronic pyelonephritisChronic pyelonephritis

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The large collection of chronic inflammatory cells here is in a patient with a history of multiple recurrent urinary tract infections. This is chronic pyelonephritis.

Glomerular disordersGlomerular disorders Due to a change or dysfunction of Due to a change or dysfunction of

the glomerular capillariesthe glomerular capillaries– Changes in membrane Changes in membrane

permeabilitypermeability– Change in GFRChange in GFR– Protein or blood cells in the urineProtein or blood cells in the urine– Systemic changes – hypertension; Systemic changes – hypertension;

edema; acid-base and electrolyte edema; acid-base and electrolyte imbalancesimbalances

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GlomerulonephritisGlomerulonephritis Caused by a number of factors, most commonly Caused by a number of factors, most commonly

abnormal immune responseabnormal immune response– InfectionInfection– Toxins Toxins – Vascular diseasesVascular diseases– Systemic diseases (diabetes mellitus)Systemic diseases (diabetes mellitus)

Can be diffuse, focal or segmentalCan be diffuse, focal or segmental Can be membranous, proliferative, sclerotic, or Can be membranous, proliferative, sclerotic, or

crecenticcrecentic Often divided into acute, rapidly progressive and Often divided into acute, rapidly progressive and

chronic forms.chronic forms.

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Acute Acute GlomerulonephritisGlomerulonephritis Often associated with streptococcal infectionOften associated with streptococcal infection Abrupt onset 7-10 days after strept throat or skin Abrupt onset 7-10 days after strept throat or skin

infection (impetigo)infection (impetigo)– Also staphylococcus or virusesAlso staphylococcus or viruses

Strept antigens deposit in glomerular basement Strept antigens deposit in glomerular basement membrane and attract neutrophils and membrane and attract neutrophils and macrophages, initiating phagocytosis and macrophages, initiating phagocytosis and release of inflammatory mediators that damage release of inflammatory mediators that damage cells on both side of the basement membrane. cells on both side of the basement membrane.

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Poststreptococcal GNPoststreptococcal GN

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Post-streptococcal glomerulonephritis is immunologically mediated, and the immune deposits are distributed in the capillary loops in a granular, bumpy pattern because of the focal nature of the deposition process.

Acute Acute GlomerulonephritisGlomerulonephritis Symptoms occur 10-21 days after infectionSymptoms occur 10-21 days after infection

– HematuriaHematuria– ProteinuriaProteinuria– Decreased GFR, oliguriaDecreased GFR, oliguria– HypertensionHypertension– Edema around eyes, feet and anklesEdema around eyes, feet and ankles– Ascites or pleural effusionAscites or pleural effusion

Biopsy – immune complexes and proliferationBiopsy – immune complexes and proliferation Most recover without significant loss of renal function or Most recover without significant loss of renal function or

recurrencerecurrence

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Rapidly Progressive GNRapidly Progressive GN

Develops over a period of days or weeksDevelops over a period of days or weeks Primarily adults in 50’s and 60’sPrimarily adults in 50’s and 60’s May be idiopathic or assoc. with a proliferative May be idiopathic or assoc. with a proliferative

diseasedisease By the time of diagnosis patient has renal By the time of diagnosis patient has renal

insufficiencyinsufficiency Proliferation of cells in Bowman’s space with crescent Proliferation of cells in Bowman’s space with crescent

formationformation Progresses to renal failure in a few weeks or monthsProgresses to renal failure in a few weeks or months Hematuria is common, may see proteinuria, edema or Hematuria is common, may see proteinuria, edema or

hypertensionhypertension

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RPGNRPGN

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This immunofluorescence micrograph of a glomerulus demonstrates positivity with antibody to fibrinogen. With a rapidly progressive GN, the glomerular damage is so severe that fibrinogen leaks into Bowman's space, leading to proliferation of the epithelial cells and formation of a crescent.

Goodpasture SyndromeGoodpasture Syndrome

Antibody formation against pulmonary and Antibody formation against pulmonary and glomerular capillary basement membranesglomerular capillary basement membranes

Activation of complement and neutrophils damage Activation of complement and neutrophils damage glomerular basement membraneglomerular basement membrane

Men 20 - 30 years of ageMen 20 - 30 years of age Pulmonary hemorrhage and renal failurePulmonary hemorrhage and renal failure

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Goodpasture SyndromeGoodpasture Syndrome Treatment must begin early or Treatment must begin early or

prognosis is poorprognosis is poor– Anticoagulants reduce fibrin Anticoagulants reduce fibrin

content of crescentscontent of crescents– Plasmapheresis with steroids and Plasmapheresis with steroids and

immunosuppression therapyimmunosuppression therapy– Dialysis or transplant if kidneys failDialysis or transplant if kidneys fail

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Goodpasture’s syndromeGoodpasture’s syndrome

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This immunofluorescence micrograph shows positivity with antibody to IgG has a smooth, diffuse, linear pattern that is characteristic for glomerular basement membrane antibody with Goodpasture's syndrome.

Chronic Chronic GlomerulonephritisGlomerulonephritis Several diseases with a progressive course Several diseases with a progressive course

leading to chronic renal failureleading to chronic renal failure Two patterns – deposition of antigen-Two patterns – deposition of antigen-

antibody complexes, or antigens specific antibody complexes, or antigens specific for GBM.for GBM.

Complement activation and phagocyte Complement activation and phagocyte activity damage wall of capillary and activity damage wall of capillary and cause proliferation of extracellular matrix, cause proliferation of extracellular matrix, affecting GFRaffecting GFR

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Chronic Chronic GlomerulonephritisGlomerulonephritis At first see increased membrane At first see increased membrane

permeability and lose cells permeability and lose cells (hematuria) or protein into urine (hematuria) or protein into urine (proteinuria)(proteinuria)

Fibrin is deposited into Bowman’s Fibrin is deposited into Bowman’s space –crescent formationspace –crescent formation

Renal blood flow and GFR is reducedRenal blood flow and GFR is reduced

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Chronic Chronic GlomerulonephritisGlomerulonephritis Clinical manifestations:Clinical manifestations:

– Hematuria – smoky brown-tinged urine Hematuria – smoky brown-tinged urine as opposed to pink or redas opposed to pink or red

– Proteinuria > 3-5 g/day mostly albuminProteinuria > 3-5 g/day mostly albumin– ↓ ↓ GFR leads to fluid retention and GFR leads to fluid retention and

hypertensionhypertension After 10 – 20 years, renal After 10 – 20 years, renal

insufficiency develops and insufficiency develops and progresses to renal failureprogresses to renal failure

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Chronic Chronic GlomerulonephritisGlomerulonephritis Treatment:Treatment:

– Treat underlying diseaseTreat underlying disease– Steroids do not change the course of the Steroids do not change the course of the

diseasedisease– Correct accompanying problems such as Correct accompanying problems such as

volume disorders, blood pressurevolume disorders, blood pressure– Ultimately dialysis or transplantUltimately dialysis or transplant

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Nephrotic SyndromeNephrotic Syndrome

Defined as excretion of 3.5 or more grams Defined as excretion of 3.5 or more grams of protein / dayof protein / day

Characteristic of glomerular injuryCharacteristic of glomerular injury Also see hypoalbuminemia, edema, Also see hypoalbuminemia, edema,

hyperlipidemiahyperlipidemia Loss of immunoglobulins can increase Loss of immunoglobulins can increase

susceptibility to infectionssusceptibility to infections

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Nephrotic SyndromeNephrotic Syndrome Treatment:Treatment:

– Diet – normal protein, low-fat, salt Diet – normal protein, low-fat, salt restrictedrestricted

– DiureticsDiuretics– ImmunosuppressionImmunosuppression– Protein supplementsProtein supplements– Removal of glomerular membrane toxic Removal of glomerular membrane toxic

factorfactor

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Renal FailureRenal Failure

Acute renal failure – abrupt decrease in renal functionAcute renal failure – abrupt decrease in renal function– Increase in BUN and creatinineIncrease in BUN and creatinine– Usually oliguria (output < 30 ml/hour or 400 ml/day)Usually oliguria (output < 30 ml/hour or 400 ml/day)– Most cases are reversible if diagnosed and treated Most cases are reversible if diagnosed and treated

earlyearly Prerenal most common cause – failure to restore Prerenal most common cause – failure to restore

blood volume or pressure and oxygen can lead to blood volume or pressure and oxygen can lead to acute tubular necrosis or acute cortical necrosisacute tubular necrosis or acute cortical necrosis

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Acute Renal FailureAcute Renal Failure Intrarenal acute renal failureIntrarenal acute renal failure

– Usually due to acute tubular necrosisUsually due to acute tubular necrosis Usually caused by ischemia most Usually caused by ischemia most

often after surgery (40 -50 %)often after surgery (40 -50 %) Also sepsis, burns, obstetrical Also sepsis, burns, obstetrical

complications, antibiotics, complications, antibiotics, radiocontrast media, other toxic radiocontrast media, other toxic substancessubstances

– Whatever the cause, decreased Whatever the cause, decreased GFR and oliguriaGFR and oliguria

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Acute Renal FailureAcute Renal Failure Postrenal acute renal failurePostrenal acute renal failure

– Usually due to urinary tract obstruction Usually due to urinary tract obstruction that affects both kidneysthat affects both kidneys

– Characterized by several hours of Characterized by several hours of anuria with flank pain, followed by anuria with flank pain, followed by polyuriapolyuria

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Acute Renal FailureAcute Renal Failure Clinical symptoms of ARF are divided Clinical symptoms of ARF are divided

into three stages:into three stages:Stage1 Oliguria:Stage1 Oliguria:

↓↓urine vol about 25 % of normal to anuriaurine vol about 25 % of normal to anuria

can last 1-3 weekscan last 1-3 weeks↑↑BUN, plasma creatinineBUN, plasma creatinine

↑ ↑ KK+ + (hyperkalemia) and electrolyte (hyperkalemia) and electrolyte imbalanceimbalance

fluid retention and edemafluid retention and edema

congestive heart failurecongestive heart failure

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Stage 2 DiuresisStage 2 Diuresis::

3-4 L/day of urine3-4 L/day of urine

Tubules still damaged, but recoveringTubules still damaged, but recovering

Can lose too much NaCan lose too much Na++ and K and K++

May see extracellular volume May see extracellular volume depletiondepletion

Stage 3 RecoveryStage 3 Recovery

May take 3-12 months for plasma May take 3-12 months for plasma creatinine to return to normalcreatinine to return to normal

About 30 % never regain normal About 30 % never regain normal kidney function.kidney function.

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Acute Renal FailureAcute Renal Failure TreatmentTreatment

– Prevention if possiblePrevention if possible– Maintain individual’s life until renal Maintain individual’s life until renal

function is recoveredfunction is recovered Correct fluid and electrolyte Correct fluid and electrolyte

imbalancesimbalances Treat infectionsTreat infections Maintain nutrition and cardiac Maintain nutrition and cardiac

functionfunction Remember drugs and/or medications Remember drugs and/or medications

are not excreted!are not excreted!6666

Chronic Renal FailureChronic Renal Failure Progressive and irreversible loss of nephronsProgressive and irreversible loss of nephrons Slow development (years)Slow development (years) Alterations in salt and water balance not apparent Alterations in salt and water balance not apparent

until renal function is less than 25% of normal.until renal function is less than 25% of normal. Common causes:Common causes:

– Chronic glomerulonephritisChronic glomerulonephritis– Chronic pyelonephritisChronic pyelonephritis

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Chronic Renal FailureChronic Renal Failure Clinical manifestations are often described Clinical manifestations are often described

using the term using the term uremia –uremia –symptoms due to symptoms due to accumulation of toxins in plasma.accumulation of toxins in plasma.– hypertensionhypertension– AnorexiaAnorexia– Nausea Nausea – Vomiting Vomiting – DiarrheaDiarrhea– Weight lossWeight loss– Pruritis (itching)Pruritis (itching)– EdemaEdema– AnemiaAnemia– Neurologic changesNeurologic changes 6868

Chronic Renal FailureChronic Renal Failure Diagnosis is by increased BUN and Diagnosis is by increased BUN and

serum creatinine; imaging will show serum creatinine; imaging will show small kidneys, and can be confirmed small kidneys, and can be confirmed by biopsyby biopsy

Management includes:Management includes:– Diet control – restrict proteins, Diet control – restrict proteins,

potassiumpotassium– Evaluate fluid and sodium levelsEvaluate fluid and sodium levels– Treat with erythropoietin as needed.Treat with erythropoietin as needed.

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