Renal Disease
I.
Classification of renal disease:
A.
For simplicity, often based on the specific structural component initially affected
by the disease:
1.
Glomerular Disease
2.
Tubular Disease
3.
Interstitial Tissue Disease
4.
Vascular Disease
B.
Over time, multiple components may be affected
II.
Glomerular Disease: (glomerulonephritis)
Most often results from damage to the basement membrane due to some type of
immunologic reaction, but can also be caused by metabolic and hereditary disorders
A.
Classification (textbook, pg 246, box 9-1)
1.
Primary glomerular disease: disease specifically affects the kidney
a.
Acute glomerulonephritis
b.
Chronic glomerulonephritis
c.
(Nephrotic syndrome)
2.
B.
Basement membrane damage
1.
Morphologic changes of the glomeruli:
a.
Cellular proliferation (in glomerular tuft)
b.
Leukocyte infiltration (especially neutrophils and macrophages)
c.
Glomerular basement membrane thickening (due to deposition of
precipitated proteins: immune complexes, fibrin)
d.
Hyalinization with sclerosis (accumulation of amorphous material;
irreversible changes)
2.
C.
Secondary glomerular disease: glomerular damage as a result of some
other disease process
a.
Systemic disease (SLE, Diabetes mellitus)
b.
Hereditary disorder (Alport’s syndrome, Fabry’s disease)
Altered glomerular function
a.
Immune complexes become entrapped in the glomeruli and bind
complement, stimulating a local inflammatory response
b.
Glomerular filtration is impaired due to inflammation of glomeruli
c.
Increased membrane permeability allows leakage of cells and
protein into urine
Clinical features indicating glomerular injury (textbook, pg 247, table 9-1)
1.
The severity and combination of symptoms depends on
a.
Number of glomeruli involved
b.
Mechanism of injury
c.
Rapidity of disease onset
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Renal and Metabolic Disease Lecture Handout
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2.
D.
Clinical findings include:
a.
Urinalysis: hematuria, proteinuria
b.
Oliguria
c.
Physical findings: edema and hypertension
d.
Blood chemistries: hypoproteinemia, azotemia (toxic condition
where increased amounts of nitrogen compounds, such as urea,
accumulate in the blood)
Types of glomerular disease (glomerulonephritis)
(textbook, pg 248, table 9-2)
1.
Acute post-streptococcal glomerulonephritis
a.
Relatively common glomerular disease; most often in children, but
can affect individuals of any age
b.
Occurs 1-2 wks following streptococcal infection of throat or skin
(group A beta-hemolytic streptococci with M-protein in cell wall)
c.
Antibody-mediated, thus blood cultures will be negative
d.
Clinical findings: sudden onset, fever, malaise, nausea, oliguria
edema (eyes, knees, ankles), mild hypertension
e.
Urinalysis:
1)
Physical and chemical exam:
2)
f.
Other testing:
Blood:
Elevated ASO titer (antistreptolysin O)
Decreased serum complement
Presence of cryoglobulins
Increased BUN, increased creatinine
Decreased plasma albumin if proteinuria large
Urine:
g.
2.
Microscopic exam
Decreased CrCl = increased / decreased GFR
Mild proteinuria: <1.0 gram/24 hr
>95% of children affected recover spontaneously or with minimal
therapy; approx 60% of adults rapidly recover. Only 1-2% of poststrep glomerulonephritis develop chronic glomerulonephritits
Chronic Glomerulonephritis (textbook, pg 251, able 9-4)
a.
Eventually, numerous (approx 80%) other glomerular diseases
result in chronic glomerulonephritis.
b.
Onset is slow and silent (insidious), taking many years to develop
signs and symptoms
CLS 426 Urine and Body Fluid Analysis: Student Lab Rotation
Renal and Metabolic Disease Lecture Handout
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c.
If not treated, may result in death from uremia (patient will need
dialysis and/or renal transplant)
d.
Clinical findings: edema, azotemia, hypertension, oliguria
e.
Urinalysis:
1)
Physical and chemical exam:
2)
f.
Other testing:
Blood:
Increased BUN, increased creatinine
Decreased plasma albumin, decreased TSP
Urine:
3.
Microscopic exam:
Decreased CrCl = increased / decreased GFR
Moderate proteinuria: >2.5 grams/24 hr
Nephrotic Syndrome (NS)
a.
Selective filtering capability of the glomerulus is lost
b.
Many conditions may lead to NS
1)
Lipoid nephritis (minimal change disease)
2)
Membranous glomerulonephritis
3)
Diabetes mellitus
6)
Malignant neoplasms
4)
SLE
7)
Infections
5)
Amyloidosis
8)
Drugs, poisons
c.
Clinical findings: soft, pitting edema, azotemia, hypertension, oliguria
d.
Urinalysis:
1)
Physical and chemical exam:
2)
e.
Microscopic exam
Other testing:
Blood:
Increased BUN, increased creatinine
Decreased plasma albumin, decreased TSP
Increased plasma lipids
Increased plasma sodium
Urine:
Decreased CrCl = increased / decreased GFR
Severe proteinuria: >3.5 grams/24 hr
CLS 426 Urine and Body Fluid Analysis: Student Lab Rotation
Renal and Metabolic Disease Lecture Handout
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4.
Diabetes Mellitus: disorder of _______________________ metabolism
a.
Complications of diabetes lead to development of diabetic
glomerulosclerosis (occurs more often in type 1 diabetes mellitus)
b.
Renal disease is the major cause of death in the diabetic patient.
Diabetes is the leading cause of
1)
Blindness in the working-age population
2)
End-stage renal disease
3)
Non-traumatic limb amputations
c.
Clinical findings: polyuria, nocturia, polydypsia
d.
Urinalysis:
1)
Physical and chemical exam:
2)
e.
Other testing:
Blood:
Increased plasma glucose (hyperglycemia)
Increased plasma ketones (type 1 DM)
Urine:
III.
Microscopic exam
Proteinuria occurs in 55% of diabetics leading to
chronic renal failure requiring dialysis or
transplantation
Tubular Disease
A.
Altered tubular function (tubular dysfunction); usually normal GFR
1.
Caused by loss of
a
Reabsorption-secretion function
b.
Concentrating-diluting function
2
Results in
a.
A build up of waste products in the blood
b.
Excessive loss of essential substances into the urine
3
Examples:
a.
Renal glycosuria: excretion of glucose into the urine, despite
normal blood glucose levels (blood glucose does not exceed renal
threshold)
b.
Cystinuria: inherited disorder, cannot reabsorb the amino acids
cystine, arginine, lysine and ornithine; cystine readily precipitates
in acid pH and can form renal calculi
c.
Cystinosis: inherited disorder, intracellular deposits of cystine
throughout the body leading to cystine crystal accumulation within
tubular cells and loss of tubular function
d.
Renal tubular acidosis: inability of tubules to secrete adequate
hydrogen ions even when systemic acidosis is present
CLS 426 Urine and Body Fluid Analysis: Student Lab Rotation
Renal and Metabolic Disease Lecture Handout
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4.
B.
Urinalysis
a.
Physical and chemical exam:
b.
Microscopic exam:
Necrosis of tubular epithelium
1.
Destruction of renal tubular epithelial cells: toxin or ischemia
2.
Most common cause of renal failure; generally, tubular damage can be
reversed once normal renal function is restored
3.
Clinical presentation often divided into 3 phases:
a.
Onset
b.
Renal failure: azotemia, hyperkalemia, metabolic acidosis, oliguria
c.
Recovery
4.
Examples:
a.
Toxic acute tubular necrosis (ATN): nephrotoxic agents that have
been injected, ingested, inhaled
1)
Drugs: antibiotics (aminoglycosides: gentamycin),
anesthetics, radiographic dyes, chemotherapy drugs,
cyclosporine
2)
Toxins: mercury, lead, cadmium, organic solvents (carbon
tetrachloride, ethylene glycol), pesticides, mushrooms
b.
5.
Ischemic ATN: follows hypotensive event that results in decreased
perfusion (blood supply) of the kidneys
1)
Sepsis: excessive bacterial infections in the bloodstream
2)
Shock: burns
3)
Trauma: crushing injuries, various surgical procedures
4)
Despite nephrotoxicity of hemoglobin and myoglobin,
ischemic ATN is caused by the dehydration and renal
ischemia that accompanies their excretion
Urinalysis
a.
Physical and chemical exam:
b.
IV.
Microscopic exam
Interstitial Tissue Disease: multiple causes
A.
Lower Urinary Tract Infection (UTI) (textbook, pg 258, table 9-8)
1.
Involves the urethra (urethritis), bladder (cystitis) or both
2.
85% UTI due to gram-negative rods present in normal feces (E.coli)
3.
Urinalysis
a.
Physical and chemical exam
b.
Microscopic exam
CLS 426 Urine and Body Fluid Analysis: Student Lab Rotation
Renal and Metabolic Disease Lecture Handout
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B.
Acute Pyelonephritis
1.
Most common upper UTI encountered
2.
3.
Bacterial infection involving renal tubules, interstitium and renal pelvis
a.
Two mechanisms can lead to this infection:
1)
Bacteria moving from lower urinary tract to kidneys (most
common cause)
2)
Bacteria in the blood (septicemia) localizing in the kidneys
b.
When voiding is incomplete, due to obstruction or dysfunction or
anatomic abnormalities, infections (bacterial proliferation) of the
kidney can occur
c.
Predisposing conditions include catheterization, urinary
obstruction, pregnancy, immunosuppressive conditions, diabetes
mellitus, patient's age and sex
Urinalysis
a.
Physical and chemical exam
b.
C.
Yeast Infections
1.
Urinary tract of both men and women is susceptible to yeast; if patient is
immuno-compromised, results in severe infections
2.
Often caused by Candida species (Candida albicans)
a.
Normal flora of GI tract and vagina
b.
Proliferation is kept in check by normal bacterial flora: antibiotic
therapy and pH changes can disrupt this normal flora, causing yeast
proliferation
c.
Has predilection for renal tissue; can cause lower or upper UTI
d.
Blood and urinary catheters provide a mode of inoculating yeast into
bloodstream or urinary tract; hospital infection?
3.
Urinalysis
a.
Physical and chemical exam
b.
V.
Microscopic exam
Microscopic exam
Vascular Disease: any disorder that affects the supply of blood to the kidneys or the
health of the renal blood vessels can cause renal disease
A.
Cardiac disease: kidney’s healthy functioning is directly related to receiving 25%
of the cardiac output
B.
Atherosclerosis of intra-renal arteries: cause reduction in renal blood flow
C.
Hypertension, diabetes, eclampsia: cause changes in arterioles and glomerular
capillaries resulting in severe and fatal renal ischemia
CLS 426 Urine and Body Fluid Analysis: Student Lab Rotation
Renal and Metabolic Disease Lecture Handout
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