MLS: AUBF LEC  Faulty abnormal protein not normall

MIDTERMS WEEK 3 – LESSON 3 produced in the body

Renal Diseases  Basement membrane thickening
Dis-ease It: A Pathologic Discussion  Assocd. with Diabetic neuropathy

Learning Objectives: Glomerular Disorders:

 Discuss the various renal diseases including their 1. ACUTE POST-STREPTOCOCCAL
pathophysiology GLOMERULONEPHRITIS (APGN)
 Discuss the physical and chemical examination of  Glomerulonephritis –definition:
renal calculi  Sterile inflammatory process that affects
 Correlate test results with pathologic conditions glomerulus and is assocd. with findings of
blood (hematuria); proteinuria and casts of
Topic Outline: your urine
1. Glomerular Diseases  Sterile –microorganisms are not the cause
2. Tubular Diseases of this process
3. Interstitial Diseases  Progressive disorder!!
4. Renal calculi  Ex. Rapidly progressive
glomerulonephritis  chronic
Types: Renal Disease glomerulonephritis  nephrotic
 Glomerular syndrome  renal failure
 1. Glomerulonephritis  Sudden condition
 A. Acute Poststreptococcal  As you’re suffering from skin and respiratory
 B. Rapidly Progressive infections caused by nephrogenic strains of
Glomerulonephritis S.pyogenes  you form IC  composed of Ag
 C. Goodpasture Syndrome coming from the organism and Ab that your system
 D. Wegener Granulomatosis produced  circulates in blood  deposited in
 E. Henoch-Schönlein Purpura glomerulus  trigges IR in glomerulus  affecting
 F. Membranous Glomerulonephritis its integrity  leading to signs and symptoms of this
 G. Membranoproliferative
disorder  inflammation (destructive process) 
Glomerulonephritis
destruction of tissues
 H. Chronic Glomerulonephritis
 I. IgA Nephropathy
 Post Infection by Group A Streptococcus
 Tubular
 Fever
 Interstitial  Periorbital edema -eyes
 Fatigue
Glomerular Disorders  Hypertension –results from increased
 May result from immunologic disorders peripheral resistance
throughout the body  Oliguria
 If there’s antigen and antigen  formation  Hematuria
of IC  can be deposited in kidneys esp in
glomerulus  attracts elements from IS   Urinalysis Results:
promotes inflammation Gross and Smoky Hematuria –urine is red!!
 Cellular infiltration/proliferation resulting to  RBC and RBC Casts
thickening of GBM (?)  Dysmorphic RBC
 Complement-mediated damage in  Indicates that bleeding is
capillaries and BM originating from glomerulus
 Bakit may complement?  Hyaline and Granular Casts
 Remember that IC has exposed Fc  Waxy Casts
portion sa Ab  attracts and  If very prolonged
eventually activates complement  WBC and WBC Cast
cascade so CS has a  Less common
participation in the inflammatory  Proteinuria and Oliguria
processes that is happening in this
GD  Other tests that can be performed:
 Clinical chemistry test
 Nonimmunologic causes:  Measurement of BUN –checks
 Exposure to chemicals and toxins renal fx
 Disruption of the electrical membrane  Serologic test –establish if there was
charges bacterial infection
 Amyloid deposition  ASO test
 And other tests
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 Glomerular Disorders: vascular walls followed by Creatinine and
2. RAPIDLY PROGRESSIVE (CRESCENTIC) producing renal BUN
damage to small involvement
GLOMERULONEPHRITIS vessels in the and possible
 More serious type lungs and progression to
glomerulus end stage
ETIOLOGY CLINICAL COURSE PRIMARY OTHER renal failure
UA RESULT SIGNIFICANT
TESTS Glomerular Disorders:
Deposition 1. Rapid onset with Macroscopic BUN 5. HENOCH-SCHÖNLEIN PURPURA
of immune glomerulardamage Hematuria
complexes and possible Creatinine
from progression to end-  Proteinuria
systemic stage renal failure Creatinine
immune Red Blood clearance
disorders 2. Crescentic Cell Casts
(SLE) on the Formation composed Deposition of
glomerular of Macro, Fibro,  GFR IgA IC in the
membrane Polymerized Fibrin = glomerulus
and often as permanent damage
complication to capillary tufts
 Raised, patchy, red lesions
of another  Common in lower extremities
form of GN  Henoch found out that:
 It is associated w GI symptoms such as
abdominal pain
 Schonlein found out that:
-biopsy  Also associated in arthritis (joint pains)

Glomerular Disorders: ETIOLOGY CLINICAL PRIMARY OTHER

3. GOODPASTURE SYNDROME COURSE UA SIGNIFICANT
RESULT TESTS
 Autoimmune disorder involving morphologic Occurs primarily Initial appearance Macroscopic Stool Occult
changes to the glomeruli similar to RPGN with in Children of purpura Hematuria Blood
autoimmune disorder following upper followed by the
 Concept of betrayal bec autoimmune :< respiratory blood in sputum Mild to
infections; a and stools and heavy
 Both BM of lungs and kidneys be affected  lung decrease in eventual renal Proteinuria
(1) and renal manifestation (2) platelets disrupts involvement
vascular integrity Red Blood
ETIOLOGY CLINICAL PRIMARY UA OTHER in the lungs and Complete Cell Casts
COURSE RESULT SIGNIFICANT glomerulus recovery –50%
TESTS
*no Others =
Attachment of Hemoptysis Macroscopic Anti-GBM
thrombocytopenia progression to
cytotoxic (coughing out Hematuria (using Px
antibody – of blood) and serum) more serious form
autoantibody dyspnea Proteinuria Of
(anti- (difficulty in glomerulonephritis
glomerular breathing) Red Blood Cell and renal failure
basement followed by Casts
membrane hematuria Glomerular Disorders:
antibody) 6. MEMBRANOUS GLOMERULONEPHRITIS (MGN)
formed after Possible
viral progression  Nephrotic in nature –leading to protein loss
infections to to CG and end  BM is involved!!
glomerular and stage
alveolar renal failure ETIOLOGY CLINICAL PRIMARY UA OTHER
basement COURSE RESULT SIGNIFICANT
membrane TESTS
Pronounced Slow Microscopic FTA-ABS –
Glomerular Disorders: thickening of progression Hematuria helps to
4. WEGENER’S GRANULOMATOSIS the glomerular with possible diagnose
basement remission Proteinuria syphilis
Causes a granuloma-producing inflammation of the small membrane If (+) = MGN
blood vessels primarily of the kidney and respiratory following IgG Nephrotic 2ndary to
system. immune syndrome syphilis
complex symptoms
ETIOLOGY CLINICAL PRIMARY UA OTHER deposition frequently AntiNA –helps
COURSE RESULT SIGNIFICANT develop – diagnose SLE
TESTS Associated protein loss and Sjogren’s
Antineutrophilic Pulmonary Macroscopic ANCA px’s with: SLE,
cytoplasmic Sjogren, 2 Thrombosis Hepatitis B
symptoms Hematuria serum
autoantibody Syphilis, Hep surface
Including Proteinuria
B, Au and Hg antigen
(ANCA) binds to hemoptysis Red Blood  serum
treatments,
neutrophils in develop first Cell Casts

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and *to establish Glomerular Disorders:
malignancy primary IGA NEPHROPATHY (BERGER DISEASE)
disorder that
may have  Most common cause esp in chilren and young
resulted to adults
MGN
ETIOLOGY CLINICAL PRIMARY UA OTHER
Glomerular Disorders: COURSE RESULT SIGNIFICANT
TESTS
7. MEMBRANOPROLIFERATIVE
Deposition Recurrent Early Stages: Serum
GLOMERULONEPHRITIS (MPGN) –Dense Deposit of IgA IC macroscopic Immunoglobulin
Disease on the hematuria Macroscopic A
 Nephritic –more inflammatory in nature glomerular following or microscopic
membrane exercise and an hematuria
 Affects both BM and mesangium!! resulting infection with
from gradual Late Stages:
ETIOLOGY CLINICAL PRIMARY OTHER increased progression to *Chronic
COURSE UA SIGNIFICANT levels chronic Glomerulonep
RESULT TESTS of serum IgA glomeruloneph hritis
Cellular Noticeable Hematuria Serum ritis and ESRD
proliferation progression to Complement **can be
(thickening) nephrotic Proteinuria Levels asymptomatic
affecting the syndrome and for many
capillary walls chronic Decreased years!!
of the glomerulonephritis complement
glomerular levels
basement because it is NEPHROTIC SYNDROME
membrane, *common in consumed bec  Has pronounced edema (manghupong)
possibly children there is  Accumulation of water in tissues
immune inflammation!
mediated
 Due to decreased protein levels in blood 
lesser oncotic pressure (pull of protein
Type 1 – against water)  water inside our BV will
increased leak out and eventually reaches peripheral
cellularity in
the
tissues
subendothelial  Bat may damage si glomerulus???
cells of the  Can be an acute onset ff instances of
mesangium circulatory disruption systemic shock
=NS

Type 2 – ETIOLOGY CLINICAL PRIMARY UA OTHER

extremely COURSE RESULT SIGNIFICANT
dense TESTS
deposits in the Increased Acute onset Marked Serum Alb
GBM =CGN permeability following Proteinuria (>3- Cholesterol
of the systemic 5g) –decreased Triglycerides
glomerular shock albumin
Glomerular Disorders: Membrane (Hypoalbuminemia)
8. CHRONIC GLOMERULONEPHRITIS due: Gradual and triggers your
 worsening symptoms include: -damage to progression liver to compensate
the from other by producing lipids
 fatigue shield of glomerular Lipiduria
 anemia negativity disorders and
 ability of the kidneys to produce -a less tightly then to Microscopic
EPO is affected fitting chronic renal Hematuria
podocyte failure
 poor stimulation in Bone Marrow to barrier RenalTubular
produce RBCs Epithelial Cells
 hypertension
 due to increased peripheral Oval Fat Bodies
resistance bec of edema Fat droplets
 edema
 oliguria; RTE, fatty, and
 decreased renal output waxy cast
 Hematuria, proteinuria, and glucosuria
 No increased blood glucose level MINIMAL CHANGE DISEASE (LIPID NEPHROSIS) or
 But there is increased glucose in the urine NIL DISEASE
 Resulted from tubular dysfunction
ETIOLOGY CLINICAL PRIMARY UA OTHER
 Broad casts, decreased GFR with increased BUN COURSE RESULT SIGNIFICANT
and Creatinine, and electrolyte imbalance TESTS
Unknown Edema Heavy Serum Albumin
-protein loss proteinuria
Cholesterol

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Disruption of Urinalysis Transient - Cyclosporine
podocytes and findings hematuria Triglyceride - Radiographic
the shield of -mawala tas dyes
negativity Frequent mubalik napd, *rationale is the - Organic solvents
occurring complete murag si…char same as NS
primarily in remission
children following Fat droplets Normal BUN
Tubular Disorders:
following corticosteroid and FANCONI’S SYNDROME
allergic treatment Creatinine (if
reactions and wala pang ETIOLOGY CLINICAL PRIMARY UA OTHER
recent progression) COURSE RESULT SIGNIFICANT
immunizations TESTS
Inherited in Generalized Glycosuria Blood glucose
Associated with association defect in
HLAB12 with the renal Mild proteinuria Serum
cystinosis tubular
FOCAL SEGMENTAL GLOMERULOSCLEROSIS and reabsorption Possible Urine electrolyte
hartnup’s (PCT) cystine
disease or requiring Crystals Amino acids
ETIOLOGY CLINICAL PRIMARY UA OTHER acquired supportive chromatography
COURSE RESULT SIGNIFICANT through therapy Low pH
TESTS exposure to
Disruption of May Mod to Heavy Drug of abuse toxic affected:
podocytes in resemble Proteinuria agents or as -glucose
certain Nephrotic HIV Test complication of -AA
areas of glomeruli syndrome Microscopic MM -phosphorous
associated with or minimal or and renal -sodium
heroin and change macroscopic transplant -potassium
analgesic disease hematuria -bicarbonate
abuse and -water
acquired
immunodeficiency
syndrome Tubular Disorders:
ALPORT SYNDROME
IgM and C3 IC  Genetic disorder showing lamellated and thinning
deposits
glomerular basement membrane
 Inherited disorder of collagen production
Tubular Disorders
 During respiratory infections, males younger the
Tubular Disorders: age of six exhibits macro hematuria then micro
ACUTE TUBULAR NECROSIS hematuria
 Ischemia –reduction of blood flow resulting in  Hearing and vision abnormalities
decreased oxygen and nutrient supplies to a tissue
Tubular Disorders:
 Shock –critical condition brought by the sudden
UROMODULIN-ASSOCIATED KIDNEY DISEASE
drop in blood flow
Ex:  Inherited disorder caused by an autosomal mutation
in the gene that produces uromodulin
 Cardiac failure –your heart fails to pump
blood  Decrease in production of normal uromodulin that is
 Sepsis replaced by the abnormal form
 Anaphylaxis  Abnormal forms accumulate in RTE cells resulting
 Massive hemorrhage to destruction
 Contact with high voltage electricity  Renal monitoring and eventual renal
 Nephrotoxic agents –can damage RTE cells transplantation
 Increase in Serum Uric Acid (SUA) leading to gout
ETIOLOGY CLINICAL PRIMARY UA OTHER as early as teenage years before onset of
COURSE RESULT SIGNIFICANT detectable renal disease
TESTS
Damaged to the Acute or Mild Hb
renal tubular cells chronic renal proteinuria
Tubular Disorders:
caused by: dysfunction Hct DIABETIC NEPHROPATHY (KIMMELSTIEL-WILSON)
usually Microscopic  Most common cause of ERD
Ischemia resolves hematuria Cardiac  Glomerular Membrane Damage
- Shock when the Enzymes –
- Trauma underlying Renal measures the  GBM thickening
- Surgical cause is Tubular integrity of the  Increased proliferation of mesangial cells
procedure corrected Epithelial heart  Increased deposition of cellular and
Cell and its noncellular material within matrix resulting
Nephrotoxic Casts And other tests
agents to accumulation of solid substances around
- Antibiotics Hyaline, capillary tuft
(aminoglycosides) Granular,  Complication of uncontrolled glucose levels in the
- Antifungals Waxy Broad
(amphotericin b) Casts
blood  proteins may be glycosylated
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  Vascular structures may develop sclerosis – *Low UTI –
affecting Increased pH
hardening of VS bladder and (alkaline)
ascending type
(if not managed ABSENCE OF
it can proceed CASTS
to Upper UT)

Interstitial Disorders:
ACUTE PYELONEPHRITIS
 Lower back pain sa may flank –affected kidneys
 Clue for diff –presence of casts!!

ETIOLOGY CLINICAL PRIMARY UA OTHER

COURSE RESULT SIGNIFICANT
TESTS
Infection of the Acute onset of Leukocyturia Urine Culture
renal tubules urinary
And interstitium Frequency of Bacteriuria Blood Culture
related to urinary
Tubular Disorders: interference of burning and WBC Casts
NEPHROGENIC DIABETES INSIPIDUS downward lower back
 Sex-linked recessive genetic disorder or acquired urine flow pain resolved Bacterial Casts
ureters to the with antibiotics
from medications including Lithium and bladder or Hematuria
Amphotericin B incomplete
 Lithium –taken as meds for bipolar emptying of the Mild Proteinuria
disorders bladder
- renal calculi
 Maybe a complication of polycystic kidney disease - reflux of urine
and SCA from the
 Decreased SG (more water less solute), pale yellow bladder to the
urine, and possible dipstick false-negatives ureters
(vesicoureteral
 Remind lang daw po ni sir k: 2 types of DI reflux),
 Nephrogenic DI
 Normal production of ADH, but Untreated
cystitis
PCT and DCT cannot respond to
the actions of ADH
 Complication of polycystic kidney Interstitial Disorders:
disease CHRONIC PYELONEPHRITIS
 Sickle cell anemia
ETIOLOGY CLINICAL PRIMARY UA OTHER
 Neurogenic DI COURSE RESULT SIGNIFICANT
 Low production of ADH TESTS
Recurrent RT Leukocyturia Urine Culture
Tubular Disorders: infection of the PERMANENT Bacteriuria
renal tubules DAMAGE and WBCcasts Blood Culture
RENAL GLYCOSURIA/GLUCOSORIA and interstitium POSSIBLE Bacterial
 Autosomal recessive glucose reabsorption defect caused mostly PROGRESSION Casts BUN
 In contrast to Fanconi, RG only affects by congenital TO Hematuria
reabsorption of glucose structural CHRONIC Proteinuria Creatinine
abnormalities RENAL Granular,
 Increase urine glucose but normal glucose in blood affecting the FAILURE Waxy, Broad Creatinine
 Inherited RG –number of glucose transporters in flow of the Clearance
PCT is decreased or the affinity of transporters to urine
glucose is decreased Frequently
diagnosed in
Interstitial Disorders Children
requires
correction
Interstitial Disorders: of the
CYSTITIS underlying
structural
ETIOLOGY CLINICAL PRIMARY UA OTHER defect
COURSE RESULT SIGNIFICANT
TESTS ACUTE INTERSTITIAL NEPHRITIS
Bacterial Acute onset of Leukocyturia Urine culture –
infection of the urinary gold standard  inflammation of the renal interstitium followed by
bladder that frequency and Bacteriuria for diagnosing inflammation of the renal tubules (adjacent)
can be burning UTI  rapid onset of symptoms relating to renal
ascending resolved with Mild Hematuria
dysfunction
antibiotics
Mildproteinuria  Oliguria –decreased renal output
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  Edema  pH –acidic, alkaline
 decreased renal concentrating ability  Chemical concentration –raw materials
 decreased GFR  Urinary Stasis –precipitation of stones
 Initial symptoms  Stones are different from crystals
 Fever
 skin rash  75% of the renal calculi composed of calcium
 Allergic reaction to medications: oxalate or phosphate
 Penicillin  Lesser percent composed of AMP, UA, Cystine
 methicillin,
 ampicillin,  Patient management techniques:
 cephalosporins,  maintaining the urine at a pH incompatible
 sulfonamides, with crystallization of the particular
 NSAIDs chemicals
 thiazide diuretics  discourage the formation of stones
 Urinalysis findings: that form/love the acid pH by
 macroscopic (probable) hematuria, mild to alkalinizing the urine, or
moderate proteinuria, numerous WBCs,  discourage the formation of stones
and WBC casts without bacteria that form/love the alkaline pH by
 Increased eosinophil acidifying the urine
 maintaining adequate hydration to lower
chemical concentration
RENAL FAILURE  suggesting possible dietary restrictions

Chronic RF  HEMATURIA -irritation to the tissues by stone

 Results from progression to other renal disease movement
 GFR of <25mL/min  Expected urinary result
 increasing BUN and creatinine  Bleeding
 clinical pictures of azotemia –can
be a result of decreased GFR RARE CALCULI
 electrolyte imbalance  Sulfonamides
 isosthenuric urine  Intake of sulfonamides + less hydration =
 lack of tubular concentrating ability sulfonamide stones
 proteinuria  Silica
 renal glycosuria  Ingested silica = precipitation
 telescoped sediments  Triamterene –mustard colored
 refers to simultaneous occurrence  Diuretic drug
of elements of chronic  Adenine
glomerulonephritis and nephrotic  inherited enzyme deficiency disorder and
syndrome hyperuricemia
 Granular cast  Xanthine
 Waxy cast  associated with a genetic disorder with an
 Broad cast absence of xanthine oxidase (enzyme that
converts xanthine to uric acid)
Acute RF:
 Can be reversible
 sudden decrease blood flow to the kidney,
acute Glomerular and Tubular disease, and
renal calculi and tumor obstructions
 many causes = varied symptoms
 Always consider primary condition that resulted to
ARF
 Generally indicated by
 decreased GFR
 oliguria
 edema Dm for corrections.
 azotemia

RENAL LITHIASIS/RENAL CALCULI/KIDNEY STONES

 may form in calices of your kidneys, ureter or
bladder
 Favorable conditions for formation: similar to
formation of urinary crystals
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