Chapter 8: Renal Disease

MTY1219 Analysis of Urine and Body Fluids Lecture [Midterm]

Mr. Nelven Gallego

OUTLINE o Rapidly progressive glomerular nephritis ->

I. Renal Disease chronic glomerulonephritis -> nephrotic
A. Classification of Renal Disease syndrome ->renal failure
II. Glomerular Disorders
A. Glomerulonephritis ACUTE POSTSTREPTOCOCCAL
B. Nephrotic Syndrome GLOMERULONEPHRITIS (AGN)
III. Tubular Disorders - Marked by the sudden onset of symptoms consistent
A. Acute Tubular Necrosis with damage to the glomerular membrane
B. Hereditary & Metabolic Disorders - Fever, edema (eyes), fatigue, hypertension, oliguria,
IV. Interstitial Disorders and hematuria
A. Tubulointerstitial Disease - Secondary complications: hypertension and
B. Acute Pyelonephritis electrolyte imbalance
C. Chronic Pyelonephritis - Children and young adults
D. Acute Interstitial Nephritis o Respiratory infections caused by certain strains
V. Renal Failure of group A streptococcus (contains M protein in
A. Acute Renal Failure the cell wall)
VI. Renal Lithiasis - Immune complexes deposit on glomerular
VII. Summary (Tables) membranes
- Urinalysis result
RENAL DISEASE o Accompanied by RBC
- Kidney’s major function o Hematuria
o Filtration of the blood to remove waste products o Proteinuria
o Oliguria
CLASSIFICATION OF RENAL DISEASE o Red blood cell (RBC) casts
- Based on the area of the kidney affected o Dysmorphic RBCs
o Glomerular Disorders o Hyaline and granular casts
o Tubular Disorders o White blood cells,
o Interstitial Disorders - Positive anti–group A streptococcal enzyme tests
o Provides evidence that the disease is of
GLOMERULAR DISORDERS streptococcal origin
- Immunologic
o Majority results from immunologic disorders RAPIDLY PROGRESSIVE (CRESCENTIC)
o Immune complexes from immunologic disorders GROMERULONEPHRITIS
o Increased serum Immunoglobulins - More serious form of AGD
§ Ex. increased IgA - Poorer prognosis
o Components of the immune system o Terminating in renal failure
§ Complement, neutrophils, lymphocytes, - Symptoms
monocytes, and cytokines o Initiated by deposition of immune complexes in
o Immune system mediators the glomerulus
§ Damage: cellular infiltration or proliferation o Complication of another form of
§ Thickening of glomerular basement glomerulonephritis
membrane o Immune systemic disorder such as systemic
§ Complement-mediated damage lupus erythematosus (SLE)
- Nonimmunologic § Macrophages damage capillary walls
o Exposure to chemicals and toxins § Fibrin = permanent damage to capillary tufts
o Deposition of amyloid material - Laboratory Results
§ Chronic Inflammation and acute phase o Urinalysis similar to AGN
reactants o More abnormal as the disease progress
o Basement Membrane Thickening § Markedly elevated protein
§ Diabetic Nephropathy § Very low glomerular filtration rate (GFR)
o Disruption of the electrical membrane charges o Increased fibrin degradation products,
as occurs in the nephrotic syndrome cryoglobulins, and the deposition of IgA immune
complexes in the glomerulus
GLOMERULONEPHRITIS
- Refers to a sterile, inflammatory process affecting GOODPASTURE SYNDROME
the glomerulus - Autoimmune disorder
- Associated with blood, protein, and casts in urine - Cytotoxic autoantibody
- May progress from one form to another

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 Chapter 8: Renal Disease
MTY1219 Analysis of Urine and Body Fluids Lecture [Midterm]
Mr. Nelven Gallego

o Appear against glomerular and alveolar MEMBRANOUS GLOMERULONEPHRITIS

basement membranes following viral respiratory - Thickening of the glomerular basement membrane
infections o Resulting from the deposition of immunoglobulin
- Antiglomerular basement membrane antibody G immune complexes
o Capillary destruction - Disorders associated
o Results from the attachment of autoantibody to o Systemic lupus erythematosus
the basement membrane followed by o Sjögren’s syndrome
complement activation o Secondary syphilis
o Detected in patient’s serum o Hepatitis B
- Initial pulmonary complaints o Gold and mercury treatments
o Hemoptysis (blood cough) and dyspnea o Malignancy
o Followed by the development of hematuria - Progression
- Urinalysis: hematuria, proteinuria, RBC casts o Slow, remission,
- Progression to Chronic glomerulonephritis to end- o Nephrotic syndrome
stage renal failure is common o possible thrombosis
- Laboratory Findings
WEGENER’S GRANULOMATOSIS o Microscopic hematuria and elevated urine
- Granuloma-producing inflammation of the small protein excretion
blood vessels § Similar to nephrotic syndrome
o Primarily of the kidney and respiratory system
- Antineutrophilic cytoplasmic antibody (ANCA) MEMBRANOPROLIFERATIVE
o Key diagnosis GLOMERULONEPHRITIS
o Seen in patient’s serum - Marked by two different alterations in the cellularity
o Initiate immune response and the resulting of the glomerulus and peripheral capillaries
granuloma formation - Type 1
- Immune response o Increased cellularity in the subendothelial cells
o Binding of ANCA and neutrophils of the mesangium (interstitial area of Bowman’s
o Produces granulomas capsule)
- Symptoms § Causing thickening of the capillary walls
o Pulmonary symptoms -> renal involvement o Progress to nephrotic syndrome
§ Hematuria, proteinuria, RBC casts, elevated - Type 2
serum creatinine and BUN o Extremely dense deposits in the glomerular
- Testing basement membrane
o incubating the patient's serum with either o Symptoms of chronic glomerulonephritis
ethanol or formalin/formaldehyde-fixed - Many of the patients are children and the disease
neutrophils has a poor prognosis.
o examining the preparation using indirect - Laboratory findings
immunofixation to detect the serum antibodies o Hematuria, proteinuria, and decreased serum
attached to the neutrophils complement levels
§ ethanol - perinuclear pattern (p-ANCA)
§ formalin/formaldehyde - granular throughout CHRONIC GLOMERULONEPHRITIS
the cytoplasm (c-ANCA) - Progression from previously discussed glomerular
disorders
HENOCH-SCHONLEIN PURPURA - Gradually worsening symptoms
- Disease occurs rapidly in children after upper o Fatigue, anemia, hypertension, edema, oliguria
respiratory infections - Urinalysis result
- Initial symptoms: Raised, red patches on skin o Hematuria, proteinuria, glucosuria (result of
- Blood in sputum and stools tubular damage), many varieties of casts (broad
- Renal involvement and waxy casts)
o Most serious complication - Markedly decreased GFR
o Mild to heavy proteinuria and hematuria with o Increased BUN and creatinine levels and
RBC casts electrolyte imbalance
- Complete recovery with normal renal function
o Seen in more than 50% of patients IMMUNOGLOBULIN A NEPHROPATHY
- Progression - Berger disease
o More serious form of glomerulonephritis and - IgA are deposited on glomerular membrane
renal failure - Most common cause of glomerulonephritis
- Patients

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 Chapter 8: Renal Disease
MTY1219 Analysis of Urine and Body Fluids Lecture [Midterm]
Mr. Nelven Gallego

o Increase serum IgA

o Episode of macroscopic hematuria following TUBULAR DISORDERS
infection or strenuous exercise - Disorders affecting the renal tubules
o May remain asymptomatic for 20 years o Tubular function is disrupted
§ Gradual progression to chronic o Result of actual damage to the tubules
glomerulonephritis - Metabolic and Hereditary Disorder affecting
functions of tubule
NEPRHOTIC SYNDROME
- Acute onset ACUTE TUBULAR NECROSIS
o Circulatory disruption - The primary disorder associated with damage to the
o Produces systematic shock renal tubules
§ Decrease the pressure and flow of blood to - Damage to the RTE cells results to Ischemia
kidney o Decrease in blood flow
- Glomerular membrane damage and changes in - Disorders causing ischemic ATN
podocyte electrical charges o Shock, trauma, surgical procedures
- Protein passes through membrane; serum albumin - Nephrotoxic agents can damage RTE cells
depleted o Aminoglycoside, antibiotics, antifungal agent
o Causing increased lipid production amphotericin B, cyclosporine, radiographic dye,
- Edema from lower oncotic pressure organic solvents (ethylene glycol, heavy metals,
- Both Tubular and glomerular damage occurs and toxic mushrooms)
- Nephrotic syndrome progress to chronic renal failure - Complete recovery
- Laboratory Findings o Correcting the ischemia, remove cause,
o Marked proteinuria >3.5 g/day managing of symptoms
o Lower levels of serum albumin -> increased lipid - Laboratory Findings
production by the liver o Mild proteinuria, microscopic hematuria
o Fat droplets, oval fat bodies, fatty casts, renal o Noticeable renal tubular epithelial (RTE) cells
tubular epithelial cells and casts, waxy casts, and casts and RTE fragments
microscopic hematuria o Result of tubular damage
§ Hyaline, waxy, granular, broad casts
MINIMAL CHANGE DISEASE
- Lipid nephrosis HEREDITARY & METABOLIC DISORDERS
- Produces little cellular change in the glomerulus - Caused by systemic conditions
o Except for some damage to podocytes and - Affect the tubular re-absorptive maximum (Tm)
shield of negativity - Failure to inherit a gene required for tubular
- Symptoms: reabsorption
o Children with edema, heavy proteinuria,
transient hematuria FANCONI SYNDROME
o Normal BUN and creatinine levels - Associated with tubular dysfunction
- Prognosis - Generalized tubular reabsorption failure in PCT
o Good, responds well with corticosteroids, - May be Inherited with cystinosis and Hartnup
frequent complete remissions disease
- Etiology = unknown - Affected function
- Allergic reactions, recent immunization, and o Dysfunction of the transport of filtered
possession of human leukocyte antigen –B12 (HLA- substances
B12) o Disruption of cellular energy
o Changes in the tubular membrane permeability
FOCAL SEGMENTAL GLOMERULONEPHRITIS - Acquired through exposure to heavy metals,
- Affects only certain numbers and areas of glomeruli outdated tetracycline
- Symptoms - Complication of multiple myeloma, renal transplant
o Similar to nephrotic syndrome - Urinalysis Findings
o Minimal change: damaged podocytes o Glycosuria with a normal blood glucose
- Immune deposits o Mild proteinuria
o IgM and C3 (frequent finding) o Low urinary pH
- Seen in association with abuse of heroin and
analgesic and with AIDS ALPORT’S SYNDROME
- Laboratory Findings - Inherited sex-linked and autosomal disorder
o Moderate to heavy proteinuria o Affecting the glomerular basement membrane
o Microscopic hematuria

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 Chapter 8: Renal Disease
MTY1219 Analysis of Urine and Body Fluids Lecture [Midterm]
Mr. Nelven Gallego

- Males inheriting as the X-linked gene are more - Either decreased number of glucose transporters in
severely affected tubules OR decreased affinity of transporters for
- Males younger than 6 years glucose
o Exhibit macroscopic hematuria with respiratory - Patients exhibit increased urine glucose
infections concentrations with normal blood glucose
- Glomerular basement membrane concentrations
o Lamellated appearance with areas of thinning
- Prognosis INTERSTITIAL DISORDERS
o Ranges from mild to persistent hematuria - Affects the tubules
o Renal insufficiency in later life to the nephrotic o Tubulointerstitial disease
syndrome and end stage renal disease - Urinary tract infection
- Cystitis
UROMODULIN-ASSOCIATED KIDNEY DISEASE
- Uromodulin TUBULOINTERSTITIAL DISEASE
o Glycoprotein - Disorders (Infections and inflammations) affecting
o Only protein produced by the kidney the interstitium and also the tubules
- Primarily an inherited disorder - Urinary Tract Infection (UTI)
o Caused by an autosomal mutation in the gene o Most common renal disease
that produces uromodulin - Cystitis (bladder infection) most frequently
- Mutation encountered
o Decrease in the production of normal uromodulin o Untreated: progresses to a more serious upper
that is replaced by the abnormal form UTI
o Increase in serum uric acid o Seen more often in women and children
§ Persons developing gout as early as the - Laboratory Findings
teenage years o Numerous WBCs, bacteria, increased pH, mild
proteinuria, hematuria
DIABETIC NEPHROPATHY o WBCs in urine called pyuria
- Currently the most common cause of end-stage
renal disease ACUTE PYELONEPHRITIS
- Damage to the glomerular membrane - Pyelonephritis
o Glomerular membrane thickening o Infection of the upper urinary tract including both
o Increased proliferation of mesangial cells tubules and interstitium
o Increased deposition of cellular and noncellular - Result of ascending movement of bacteria from a
material within matrix lower UTI into the renal tubules and interstitium
o Associated with deposition of glycosylated o Conditions affecting emptying of bladder
proteins resulting from poorly controlled blood § Calculi, pregnancy, reflux of urine from
glucose level bladder to ureters
§ Sclerosis of vascular structure - Patients present with rapid onset, urinary frequency,
§ Reason for early microalbumin testing burning on urination and lower back pain
- Laboratory Findings
NEPHROGENIC DIABETES INSIPIDUS o Similar to cystitis (numerous WBCs and bacteria
- Two types of Diabetes Insipidus with mild proteinuria and hematuria)
o Nephrogenic: failure of tubules to respond to o additional finding: presence of WBC casts
antidiuretic hormone (ADH), inherited sex-linked
recessive or medication such as lithium and CHRONIC PYELONEPHRITIS
amphotericin B, polycystic kidneys and sickle - Serious disorder resulting in permanent damage to
cell anemia the renal tubules
o Neurogenic: failure to produce ADH o Progression to chronic renal failure
- Urinalysis findings for Diabetes Insipidus - Congenital urinary structural defects causing reflux
o Low specific gravity nephropathy
o Pale yellow color - Can affect emptying of collecting ducts
o Possible false negative results for chemical tests - Often diagnosed in children
- Laboratory Findings
RENAL GLYCOSURIA o Similar to acute pyelonephritis (early stages)
- Affects only the reabsorption of glucose o Later granular, waxy, and broad casts
- Inherited as an autosomal recessive trait § Increased protein, hematuria, and
decreased renal concentration (specific
gravity)

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 Chapter 8: Renal Disease
MTY1219 Analysis of Urine and Body Fluids Lecture [Midterm]
Mr. Nelven Gallego

- Postrenal
ACUTE INTERSTITIAL NEPHRITIS o Normal- and abnormal-appearing urothelial cells
- Marked by inflammation possibly associated with malignancy
- Renal interstitium -> renal tubules § Renal calculi
- Rapid onset of symptoms relating to renal § Tumors
dysfunction
o Oliguria, edema, decreased renal concentration RENAL LITHIASIS
- Fever and skin rash – frequent initial symptoms - Renal calculi (kidney stones)
- Medication allergy to penicillin, methicillin, ampicillin, o Form in the calyces and pelvis of kidney,
cephalosporins, NSAIDs, thiazide diuretics; ureters, and bladder
discontinue; use steroids - Staghorn calculi
- Urinalysis, hematuria, proteinuria, Numerous WBCs, o Resembling the shape of the renal pelvis
WBC casts, NO BACTERIA o Smooth, round bladder stone with diameter of 2
- Develop approximately 2 weeks following or more inches
administration of medication o Vary in size (barely visible to large)
- Initial symptoms: fever and the presence of a skin - Small calculi may be passed in the urine
rash o Severe back pain radiating from lower back to
- Confirmation: Differential leukocyte staining for the legs when passing
presence of increased eosinophils - Lithotripsy:
o Procedure
RENAL FAILURE o High energy shock waves break up stones
- Exists in both acute and chronic forms o Stones can also be removed surgically
- Chronic renal failure o Calculus formation
- Progression from original disorders to end-stage § Finding of clumps of crystals in freshly
renal disease voided urine
- Marked decrease to GFR (less than 25mL/min), - Formation conditions similar to crystals
steadily rising serum BUN and creatinine levels o pH, concentration, stasis
(azotemia), electrolyte imbalance, isosthenuric urine, o Increased in the summer
proteinuria, renal glycosuria, and an abundance of - Types of stones
granular, waxy, broad casts o 75% calcium oxalate or phosphate
o Magnesium ammonium phosphate (struvite)
ACUTE RENAL FAILURE § UTI and ↑ pH, like triple phosphate crystals
- Sudden loss of renal function o Uric acid: increased purine diet
- Frequently reversible o Cystine: hereditary cystinosis
- Causes - Primary calculi constituents
o Sudden decreased blood flow (prerenal) o Magnesium ammonium phosphate (struvite)
o Acute glomerular and tubular disease (renal) § Frequently accompanied by urinary
o Renal calculi and tumors (postrenal) infections involving urea-splitting bacteria
- Urinalysis findings are varied (related to cause) o Uric acid
o RTE cells and casts = prerenal origin § Associated with increased intake of foods
o RBCs = glomerular injury with high purine content and with
o WBCs and casts = infection/inflammation of uromodulin-associated kidney disease
renal origin o Cystine
o urothelial cells = possible malignancy § Seen in conjunction with hereditary
disorders of cystine metabolism
CAUSES OF ACUTE RENAL FAILURE o Calcium canaliculi
- Prerenal § Metabolic calcium and phosphate disorders
o Sudden decrease in blood flow to the kidney and occasionally diet
§ Decreased blood pressure/cardiac output
§ Hemorrhage
§ Burns
§ Surgery
§ Septicemia
- Renal
o Acute glomerulonephritis
o Acute tubular necrosis
o Acute pyelonephritis
o Acute interstitial nephritis

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 Chapter 8: Renal Disease
MTY1219 Analysis of Urine and Body Fluids Lecture [Midterm]
Mr. Nelven Gallego

SUMMARY

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Chapter 8: Renal Disease
MTY1219 Analysis of Urine and Body Fluids Lecture [Midterm]
Mr. Nelven Gallego

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