TRANS:

AUBF
● Acue glomerulonephritis to chronic glomerulonephritis to
nephrotic syndrome to renal failure.

LECTURE ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS

CHAPTER 7: RENAL DISEASE ● Fever, edema around the eyes, oliguria, and hematuria

● Immune complexes deposit on the glomerular membranes

Disorders throughout the body can affect renal function and
produce abnormalities in the urinalysis. ● Hematuria, proteinuria, oliguria
The kidneys are consistently exposed to potentially damaging - Red blood cell (RBC) casts, dysmorphic RBCs
substances. - Hyaline and granular casts
- White blood cells
- Anti-group A streptococcal enzyme tests
CLASSIFICATION  A streptococcal infection from organisms with M protein in
the cell wall
 Glomerular disorders  Rapid anti-group A streptococcal enzyme tests
 Tubular disorders - Ease in diagnosis
 Interstitial disorders - Decline in incidence

GLOMERULAR DISORDERS RAPIDLY PROGRESSIVE (CRESCENTIC)

GLOMERULONEPHRITIS
Majority are of immunologic disorders.
● Immune complexes from immunologic reactions ● More serious form renal failure
throughout the body
● Systematic immune disorders
● Increased serum immunoglobulins are deposited on the - Macrophages damage capillary walls
glomerular membranes. - Fibrin = permanent damage to capillary tufts
● Immune system mediators: complement migrate and ● Urinalysis similar AGN progresses to more abnormal,
produce change and damage to membranes. elevated protein, low glomerular filtration rate (GFR)
Nonimmunologic
● May have increased fibrin degradation product (FDP),
● Chemicals and toxins, deposition of amyloid material and Cryoglobulins and IgA immune complex depositions
acute phase, electrical charge interference, membrane
thickening. GOODPASTURE’S SYNDROME

● Morphological changes resembling crescentric GN

● Autoimmune disorder against glomerular and alveolar

basement membranes
● Cytotoxic antibody following viral respiratory diseases
- Antiglomerular basement membrane antibody
 Hemoptysis, hematuria, proteinuria, RBC casts
 Chronic Glomerulonephritis to end-stage renal failure is
common.

WEGENER’S GRANULOMATOSIS

● Inflammation and granulomas in small blood vessels of

kidney and respiratory system
GLOMERULAR DISORDERS ● Key diagnosis:
- Antineutrophilic cytoplasmic antibody (ANCA)
Glomerulonephritis
● Neutrophils initiate immune responnse, producing
● General term of sterile, inflammatory process affecting the
granulomas.
glomerulus.  Pulmonary symptoms first, then hematuria, proteinuria,
● Causes blood, protein, and casts in urine. RBC casts, elevated BUN and creatinine levels
 Immunofixation of p-ANCA/c-ANCA
Type of glomerulonephritis progress through various
disorders HENOCH-SCHOLEIN PURPURA

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● Children following upper respiratory infections

● Raised, red patches on the skin

● Blood in sputum and possible stools

● Renal involvement is the most serious complication if the

disorder
- Proteinuria and hematuria, RBCs casts
● 50% complete recovery

● Follow patients for more serious renal problems

IMMUNOGLOBULINS A NEPHROPATHY (BERGER’S DISEASE)
MEMBRANOUS GLOMERULONEPHRITIS
● Most common cause of glomerulonephritis
● IgG immune complexes cause pronounced thickening on
the glomerular basement membrane ● IgA complexes on glomerular membrane

● Systemic lupus erythematous, Sjorgen’s syndrome, ● Increase serum IgA

secondary syphilis, hepatitis B, gold and mercury ● Early macroscopic hematuria from exercise or infections
treatments, malignancy
- These aids diagnosis with spontaneous recovery
- Often unknown etiology ● 20 years later: gradual progression to chronic
 Slow progression, remission, nephrotic syndrome glomerulonephritis
 Microscopic hematuria, very high protein
● Granular and disintegrating RBC casts
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
(MPGN) NEPHROTIC SYNDROME

● Type !: increased cellularity in the subendothelial cell of ● Acute onset from systemic shock (low blood pressure) or
the mesangium glomerulonephritis complication
- Thickening of the capillary walls
● Glomerular membrane damage and changes in podocyte
● Type 2: extremely dense deposits in the glomerular electrical charges
basement membrane
● Protein passes through membrane; serum albumin
- Poor diagnosis
depleted, causing increased lipid production
● Hematuria, proteinuria, complement
● Edema from loss of oncotic pressure
● Autoimmune disorders, infections, malignancies
● Tubular damage
CHRONIC GLOMERULONEPHRITIS
URINALYSIS
● Progression from previous disorders
 Marked proteinuria
● Fatigue, anemia, hypertension, edema, oliguria gradually >3.5 g/day
 Fat droplets, oval fat
worsening
bodies, fatty casts,
● Hematuria, Proteinuria, glycosuria (tubular damage), many renal tubular epithelial
types of casts including broad and waxy casts cells and casts, waxy
casts, microscopic
● Markedly decreased GFR hematuria

MINIMAL CHANGES DISEASE

(LIPID NEPHROSIS)

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● Children, allergic reactions, immunization, HLA-B12
● Heavy proteinuria, edema, transient hematuria; normal
BUN and creatinine levels
● Good prognosis, steroids, remission
FOCAL SEGMENTAL GLOMERULONEPHRITIS
● Similar to nephrotic syndrome but affects only certain
numbers and areas of glomeruli; podocytes are damaged
● IgM and C3 immune deposits
● Moderate to heavy proteinuria; microscopic hematuria
● Heroin and analgesic abuse, HIV
ACUTE TUBULAR NECROSIS
● Similar to nephrotic syndrome but affects only certain
numbers and areas of glomeruli; podocytes are damaged
● Ischemia: severe decrease in blood flow
- Trauma, surgery, cardiac failure, electricity, toxogenic
bacteria, anaphylaxis
● Nephrotoxic agents: aminoglycosides, amphotericin B,
ethylene glycol, heavy metals, mushroom poisoning,
hemoglobin, myoglobin
● Remove cause and manage symptoms
● Noticeable renal tubular epithelial (RTE) cells and casts
and RTE fragments
● Hyaline, waxy, granular, broad casts
ALPORT’S SYNDROME
● Inherited sex-linked and autosomal disorder affecting
basement membrane
● Males more severely affected
● Macroscopic hematuria with respiratory infections by age
6 years
● Membrane laminated with thinning; no immune complexes
● Mild to persistent hematuria, later nephrotic syndrome,
renal failure for some
UROMODULIN ASSOCIATED KIDNEY DISEASE (UMKD)
● Formerly Tamm-Horsfal protein is the only protein
produced by the kidney
● Inherited disorder that results in an abnormal buildup of
uromodulin in the tubular cells causing their destruction
● Patients have elevated serum uric acid and gout at an
early age, occurs before renal symptoms
DIABETIC NEPHROPATHY
● Most common cause of end-stage renal disease
● Glomerular basement membrane thickening
● Increased proliferation of mesangial cells
● Increased deposition of cellular and acellular material
within matrix of Bowman’s capsule and around capillary
tufts
● Deposition associated with glycosylated proteins from
poorly controlled diet
● Sclerosis of vascular structure
● Reason for early microalbumin testing
HEREDITARY AND METABOLIC DISORDERS
● Fanconi syndrome
- Generalized proximal convoluted tubule reabsorption
failure
- Inherited with cystinosis and Hartnup disease
- Acquired: heavy metals, outdated tetracycline
- Complication of multiple myeloma, renal transplant
- Glycosuria and electrolyte imbalance
NEPHROGENIC DIABETES INSIPIDUS
● Two types
1. Nephrogenic: failure of tubules to respond to antidiuretic
hormone (ADH), inherited sex-linked recessive or lithium
and amphotericin B exposure, polycystic kidneys and
sickle cell anemia
2. Neurogenic: failure to produce ADH
 Urine: pale yellow, low specific gravity (SG), possible
negative results for other tests
RENAL GLYCOSURIA
● Affects only the reabsorption of glucose
● Inherited as autosomal recessive
● Decreased number of glucose transporters in tubules
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● Decreased affinity of transporters for glucose

● Glycosuria with normal blood glucose level

TUBULOINTERSTITIAL DISEASES

● Infections and inflammations affecting the interstitium and

the tubules
● Most common renal disease is urinary tract infection (UTI)

● Cystitis (bladder infection) is very common

- Untreated: progresses to upper urinary tract RENAL FAILURE
- Many WBCs, bacteria, increased pH, mild proteinuria,
hematuria
- WBCs in urine called pyuria
● Acute and chronic forms
ACUTE PYELONEPHRITIS
● Chronic renal failure
- Progression from original disorders to end-stage
● Ascending movement of bacteria renal disease
- GFR <25 mL/min, ↑↑ BUN and creatinine levels,
- Conditions affecting emptying of bladder
electrolyte imbalance, isosthenuria, proteinuria, renal
- Calculi, pregnancy, reflux of urine from bladder to
ureters glycosuria; ↑ granular, waxy, broad casts
● Rapid onset, urinary frequency, burning, lower back pain ACUTE RENAL FAILURE
● Urinalysis: similar to cystitis with one exception: presence
of WBC casts
● Sudden onset, often reversible
CHRONIC PYELONEPHRITIS ● Decreased blood flow (prerenal), acute disease (renal),
renal calculi and tumors (postrenal)

● Damage to tubules, possible renal failure ● Urinalysis related to cause

- RTE cells = decreased blood flow
● Congenital structural defects causing reflux are most - RBCs = glomerular damage
common cause - WBCs and casts = infection/inflammation
- Urothelial cells = possible bladder tumor
● Can affect emptying of collecting ducts

● Often diagnosed in children CAUSES OF ACUTE RENAL FAILURE

● Early urinalysis similar to acute pyelonephritis

● Later granular, waxy, and broad casts; increased protein, ● Prerenal

hematuria, ↓ SG - Decreased blood pressure/cardiac output
- Hemorrhage
- Burns
ACUTE INTERSTITIAL NEPHRITIS - Surgery
- Septicemia
 Renal
- Acute glomerulonephritis
● Allergic reaction causing inflammation of interstitium and - Acute tubular necrosis
tubules - Acute pyelonephritis
- Acute interstitial nephritis
● Medication allergy to penicillin, methicillin, ampicillin,
● Postrenal
cephalosporins, NSAIDs, thiazide diuretics
- Renal calculi
● Discontinue and use steroids to treat - Tumors
- Crystallization of ingested substances
● Urinalysis, hematuria, proteinuria,↑ WBCs, WBC casts, no
bacteria RENAL LITHIASIS
● Hansel stain for eosinophils

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● Renal calculi (kidney stones) in calyces and pelvis of

kidney, ureters, bladder
● Staghorn, round and smooth, barely seen

● Severe back pain radiating from lower back to legs when

passing
● Lithotripsy: high-energy shock waves break up stones

● Also surgical removal

● Formation conditions similar to crystals

- pH, concentration, urine stasis
- No exact cause of formation known
- Increased in the summer, dehydration
 Types of stones
- 75% calcium oxalate or phosphate
- Magnesium ammonium phosphate (stuvite)
• UTI and ↑ pH, like triple phosphate crystals
- Uric acid: increased purine diet
- Cystine: hereditary cystinosis