Transcript renal disease - 36-454-f10

RENAL DISEASE
CHAPTER 7
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Learning Objectives
Upon completing this chapter, the reader will be able to
1. Differentiate among renal diseases of glomerular, tubular, interstitial,
and vascular origin.
2. Describe the processes by which immunologic damage is caused to
the glomerular basement membrane.
3. Define glomerulonephritis.
4. Describe the characteristic clinical symptoms, etiology, and urinalysis
findings in acute poststreptococcal and rapidly progressive
glomerulonephritis, Goodpasture syndrome, Wegener’s
granulomatosis, and Henoch-Schönlein purpura.
5. Name three renal disorders that also involve acute respiratory
symptoms.
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Learning Objectives (cont’d)
6.
Differentiate between membranous and membranoproliferative
glomerulonephritis.
7. Discuss the clinical course and significant laboratory results associated
with immunoglobulin A nephropathy.
8. Relate laboratory results associated with the nephrotic syndrome to
the disease process.
9. Compare and contrast the nephrotic syndrome and minimal change
disease with regard to laboratory results and course of disease.
10. State two causes of acute tubular necrosis.
11. Name the urinary sediment constituent most diagnostic of renal
tubular damage.
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Learning Objectives (cont’d)
12. Describe Fanconi syndrome, Alport syndrome, uromodulinassociated renal disease, and renal glucosuria.
13. Differentiate between diabetic nephropathy and nephrogenic
diabetes insipidus.
14. Compare and contrast the urinalysis results in patients with
cystitis, pyelonephritis, and acute interstitial nephritis.
15. Differentiate among causes of laboratory results associated
with prerenal, renal, and postrenal acute renal failure.
16. Discuss the formation of renal calculi, composition of renal
calculi, and patient management techniques.
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Introduction
• Disorders throughout the body can affect renal
function and produce abnormalities in the
urinalysis
• The kidneys are consistently exposed to
potentially damaging substances
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Classification
• Glomerular disorders
• Tubular disorders
• Interstitial disorders
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Glomerular Disorders
• Majority are of immunologic disorders
– Immune complexes from immunologic reactions
throughout the body
– Increased serum immunoglobulins are deposited on the
glomerular membranes
– Immune system mediators: complement migrate and
produce change and damage to membranes
• Nonimmunologic
– Chemicals and toxins, deposition of amyloid material and
acute phase reactants, electrical charge interference,
membrane thickening
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Glomerular Disorders (cont’d)
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Glomerular Disorders (cont’d)
• Glomerulonephritis
– General term for sterile, inflammatory process
affecting the glomerulus
– Causes blood, protein, and casts in urine
• Types of glomerulonephritis progress through
various disorders
– Acute glomerulonephritis to chronic
glomerulonephritis to nephrotic syndrome to renal
failure
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Acute Poststreptococal
Glomerulonephritis (AGN)
• Fever, edema around the eyes, oliguria, and hematuria
• Immune complexes deposit on glomerular membranes
• Hematuria, proteinuria, oliguria
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Red blood cell (RBC) casts, dysmorphic RBCs
Hyaline and granular casts
White blood cells
Anti–group A streptococcal enzyme tests
• Group A streptococcal infections from organisms with M
protein in the cell wall
• Rapid anti–group A streptococcal enzyme tests
– Ease in diagnosis
– Decline in incidence
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Rapidly Progressive (Crescentic)
Glomerulonephritis
• More serious acute form → renal failure
• Systemic immune disorders
– Macrophages damage capillary walls
– Fibrin = permanent damage to capillary tufts
• Urinalysis similar to AGN progresses to more abnormal,
elevated protein, low glomerular filtration rate (GFR)
• May have increased fibrin degradation products (FDP),
cryoglobulins and IgA immune complex depositions
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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
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Wegener’s Granulomatosis
• Inflammation and granulomas in small blood vessels of
kidney and respiratory system
• Key to diagnosis
– Antineutrophilic cytoplasmic antibody (ANCA)
• Neutrophils initiate immune response, producing
granulomas
• Pulmonary symptoms first, then hematuria, proteinuria,
RBC casts, elevated BUN and creatinine levels
• Immunofixation for p-ANCA/c-ANCA
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Henoch-Schönlein Purpura
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Children following upper respiratory infections
Raised, red patches on skin
Blood in sputum and possibly stools
Renal involvement is the most serious complication
of the disorder
– Proteinuria and hematuria, RBC casts
• 50% complete recovery
• Follow patients for more serious renal problems
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Membranous Glomerulonephritis
• IgG immune complexes cause pronounced
thickening on glomerular basement membrane
• Systemic lupus erythematosus, Sjögren’s syndrome,
secondary syphilis, hepatitis B, gold and mercury
treatments, malignancy
– These aid in diagnosis
– Often unknown etiology
• Slow progression, remission, nephrotic syndrome
• Microscopic hematuria, very high protein
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Membranoproliferative
Glomerulonephritis (MPGN)
• Type 1: increased cellularity in the
subendothelial cells of the mesangium
– Thickening of capillary walls
• Type 2: extremely dense deposits in the
glomerular basement membrane
– Poor prognosis
• Hematuria, proteinuria, ↓ complement
• Autoimmune disorders, infections, malignancies
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Chronic Glomerulonephritis
• Progression from previous
disorders
• Fatigue, anemia,
hypertension, edema,
oliguria gradually worsening
• Hematuria, proteinuria,
glycosuria (tubular
damage), many types of
casts including broad and
waxy casts
• Markedly decreased GFR
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Immunoglobulin A Nephropathy
(Berger’s Disease)
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•
Most common cause of glomerulonephritis
IgA complexes on glomerular membrane
Increase serum IgA
Early macroscopic hematuria from exercise or
infection with spontaneous recovery
• 20 years later: gradual progression to chronic
glomerulonephritis
• Granular and disintegrating RBC casts
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Nephrotic Syndrome
• Acute onset from systemic shock (low blood
pressure) or glomerulonephritis complication
• Glomerular membrane damage and changes in
podocyte electrical charges
• Protein passes through membrane; serum albumin
depleted, causing increased lipid production
• Edema from loss of oncotic pressure
• Tubular damage
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Urinalysis
• Marked proteinuria
>3.5 g/day
• Fat droplets, oval fat
bodies, fatty casts, renal
tubular epithelial cells
and casts, waxy casts,
microscopic hematuria
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Minimal Change Disease
(Lipid Nephrosis)
• Children, allergic reactions, immunization, HLAB12
• Heavy proteinuria, edema, transient hematuria;
normal BUN and creatinine levels
• Good prognosis, steroids, remission
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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
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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
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Uromodulin Associated Kidney
Diseases (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
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Diabetic Nephropathy
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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
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Acute Tubular Necrosis
• 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
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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
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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
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Renal Glycosuria
• Affects only the reabsorption of glucose
• Inherited as autosomal recessive
• Decreased number of glucose transporters in
tubules
• Decreased affinity of transporters for glucose
• Glycosuria with normal blood glucose level
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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
– Many WBCs, bacteria, increased pH, mild proteinuria,
hematuria
– WBCs in urine called pyuria
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Acute Pyelonephritis
• Ascending movement of
bacteria
– Conditions affecting emptying
of bladder
– Calculi, pregnancy, reflux of
urine from bladder to ureters
• Rapid onset, urinary
frequency, burning, lower
back pain
• Urinalysis: similar to cystitis
with one exception:
presence of WBC casts
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Chronic Pyelonephritis
• Damage to tubules, possible renal failure
• Congenital structural defects causing reflux are
most common cause
• Can affect emptying of collecting ducts
• Often diagnosed in children
• Early urinalysis similar to acute pyelonephritis
• Later granular, waxy, and broad casts; increased
protein, hematuria, ↓ SG
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Acute Interstitial Nephritis
• Allergic reaction causing
inflammation of interstitium
and tubules
• Medication allergy to
penicillin, methicillin,
ampicillin, cephalosporins,
NSAIDs, thiazide diuretics
• Discontinue and use
steroids to treat
• Urinalysis, hematuria,
proteinuria,↑ WBCs, WBC
casts, no bacteria
• Hansel stain for eosinophils
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Renal Failure
• Acute and chronic forms
• Chronic renal failure
– Progression from original disorders to end-stage renal
disease
– GFR <25 mL/min, ↑↑ BUN and creatinine levels,
electrolyte imbalance, isosthenuria, proteinuria, renal
gycosuria; ↑ granular, waxy, broad casts
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Acute Renal Failure
• Sudden onset, often reversible
• Decreased blood flow (prerenal), acute disease
(renal), renal calculi and tumors (postrenal)
• Urinalysis related to cause
– RTE cells = decreased blood flow
– RBCs = glomerular damage
– WBCs and casts = infection/inflammation
– Urothelial cells = possible bladder tumor
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Causes of Acute Renal Failure
• Prerenal
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Decreased blood pressure/cardiac output
Hemorrhage
Burns
Surgery
Septicemia
• Renal
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Acute glomerulonephritis
Acute tubular necrosis
Acute pyelonephritis
Acute interstitial nephritis
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Causes of Acute Renal Failure (cont’d)
• Postrenal
– Renal calculi
– Tumors
– Crystallization of ingested substances
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Renal Lithiasis
• 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
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Renal Lithiasis (cont’d)
• 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
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