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Urinalysis > Kidney Function > Flashcards

Kidney Function Flashcards

1
Q

Acute Glomerulonephritis

A

Hematuria, proteinuria, and oliguria. Also seen are RBC casts, dysmorphic RBCs, hyaline and granular casts and WBCs. BUN may be elevated. May demonstrate a positive ASO titer. Cloudy, red, positive protein and blood.

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2
Q

Discuss the pathogenesis of this condition and the projected outlook for the patient.

A

Damage to the glomerular membrane. Symptoms include fever; edema, fatigue, hypertension, oliguria, and hematuria. Usually occur in children and young adults following group A Streptococcus infections. . The Streptococcus organisms form immune complexes with their corresponding circulating antibodies and causes glomerulonephritis.

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3
Q

Discuss the anatomy and physiology of the glomerulus.

A

The glomerulus consists of a coil of approximately eight capillary lobes known as the capillary tuft that is housed within the Bowman’s capsule.

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4
Q

Rapid Progressive glomerulonephritis(RPGN) crescentic glomerulonephritis

Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests

A

Pathogenesis: antibody mediated often antibodies to the glomerular basement membrane

Glomerular changes: the cells of the Bowman’s space form crescents; leukocytic infiltration; fibrin deposits, GBM disruption

Urinalysis: gross hematuria, proteinuria, and RBC casts.

Chemistry Tests: increased BUN, Creatinine, decrease creatinine clearance

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5
Q

Membaranous glomerulonephritis(MGM)

Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests

A

Pathogenesis: Antibody mediated

Glomerular changes: basement membrane thickens as a result of antibodies and complement deposits, loss of foot cell processes

Urinalysis: RBC’s, proteinuria

Chemistry Tests: Antinuclear antibodies, hepatitis B antigens, FTA-ABS

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6
Q

Membranoproliferative glomerulonephritis(MPGN)

Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests

A

Pathogenesis: Immune complex or complement activation

Glomerular changes: cellular proliferation of the mesangium, leukocytic infiltration, IgG and complement deposits

Urinalysis: RBC’s, proteinuria

Chemistry Tests: increased serum compliment levels

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7
Q

Chronic Glomerulonephritis

Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests

A

Pathogenesis: Variable

Glomerular changes: hyalinized glomeruli

Urinalysis: RBC’s, hematuria, proteinuria, glucosuria and granular, waxy, and broad casts

Chemistry Tests: decreased glomerular filtration rate and an increased BUN and creatinine levels. Electrolyte imbalance.

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8
Q

IgA nephropathy

Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests

A

Pathogenesis: IgA mediated; compliment activation

Glomerular changes: Deposits of IGA in mesangium, variable cellular proliferation

Urinalysis: Early stages hematuria. Late stages RBC’s, hematuria, proteinuria, glucosuria and granular, waxy, and broad casts

Chemistry Tests: increased serum IgA

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9
Q

Focal segmented glomerulosclerosis(FSGS)

Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests

A

Pathogenesis: Unknown possibly a circulating systemic factor; can reoccur after kidney transplant

Glomerular changes: sclerotic glomeruli with hyaline and lipid deposits(focal and segmental) diffuse loss of foot processes; focal IgM and C3 deposits

Urinalysis: RBC’s, proteinuria

Chemistry Tests: drug testing and genetic testing.

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10
Q

Pyelonephritis

Macroscopically
Microscopically

A

Macroscopically-cloudy urine, protein, blood, nitrites, leukocyte esterase
Microscopically-WBCs, renal epithelial cells, WBC casts, moderate bacteria

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11
Q

Proximal tubule

Mode of Reabsorption and Substance

A

Passive - H2O, Cl-, K+, urea

Active - Na+, HCO3-, glucose, proteins, phosphate, sulfate, Mg+, Ca2+, uric and amino acids

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12
Q

Loop of Henle

Mode of Reabsorption and Substance

A

Thin descending - Passive - H2O, urea

Loop of Henle - Passive - Na+, Cl-, urea

Thick ascending(medullary and cortical) - Passive - urea
                                                                      Active - Na+, Cl-
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13
Q

Distal Tubule (convoluted portion)

Mode of Reabsorption and Substance

A

Passive - H2O

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14
Q

Collecting Tubules

Mode of Reabsorption and Substance

A

Cortical Passive - H2O, Cl-
Active - Na+

Medullary Passive - H2O, urea

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15
Q

Discuss where the ultrafiltrate components are secreted in the nephron.

Proximal Tubule
Loop of Henle
Distal Tubule
Collecting Tubules

A

Proximal tubule - H+, NH3, weak acids and bases

Loop of Henle - Urea

Distal Tubule (convoluted portion) - H+, NH3, K+, uric acid

Collecting Tubules - H+, NH3, K+

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16
Q

Acute Pyelonephritis

Physical and Chemical Examination
Microscopic Examination

A 
Physical and Chemical Examination
Protein: small(<1.0 g/day)
Blood: positive(usually small)
Leukocyte esterase: positive
Nitrite: positive
Specific Gravity: normal to low

Microscopic exam
WBCs clumps, Bacteria (GNR), RBC’s, Renal epithelial cells, WBC, granular, renal cellular, waxy casts

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17
Q

Chronic Pyelonephritis

Physical and Chemical Examination
Microscopic Examination

A

Physical and Chemical Examination
Protein: moderate(2.5 g/day)
Leukocyte esterase: positive
Specific Gravity: low

Microscopic exam
WBCs, WBC, granular, renal cellular, waxy, broad casts

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18
Q

Acute interstitial nephritis

Physical and Chemical Examination
Microscopic Examination

A

Physical and Chemical Examination
Protein: mild(~1 g/day)
Blood: positive
Leukocyte esterase: positive

Microscopic exam
WBCs Increased eosinophils , RBC’s, Renal epithelial cells, WBC, granular, renal cellular, waxy, broad casts

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19
Q

Cystitis

Physical and Chemical Examination
Microscopic exam

A 
Physical and Chemical Examination	
Protein: small(<0.5 g/day)
Blood: positive(usually small)
Leukocyte esterase: positive
Nitrite: positive

Microscopic exam
WBCs, Bacteria, RBC’s, Transitional epithelial cells

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20
Q

Nephrotic syndrome

Macroscopic and Microscopic

A

Macroscopically: cloudy/foamy urine, large amount of protein, small amount of blood

Microscopically: renal cells and hematuria, granular, waxy, fatty casts, oval fat bodies, urinary fat droplets, renal tubular epithelial cells, epithelial, renal, fatty, and waxy casts,

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21
Q

Discuss the disease process of nephrotic syndrome

A

Clinical features that happen all at once and can happen as a result of glomerulonephritis, circulatory shock , or decreased blood flow to the kidney. Massive proteinuria >3.5, low serum albumin and high serum lipids

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22
Q

BUN

Definition and reference range

A

BUN or Blood Urea Nitrogen: Is the amount of nitrogen found in the blood from breakdown of Urea which is filtered by the glomerulus. Most of it is excreted in the urine however 40% is reabsorbed in the renal tubules.

BUN: 6-20 mg/dL

23
Q

Creatinine

Definition and reference range

A

Creatinine is the breakdown product of creatine phosphate in muscle and is released into the circulation at a constant rate and is directly proportional to a person’s muscle mass. Creatinine is filtered by the glomerulus and excreted in the urine.

Females-0.5-0.8 mg/dL
Males-0.6-1.1 mg/dL

24
Q

BUN creatinine ratio

Definition and reference range

A

The BUN creatinine ratio compares the two results and used to determine either acute kidney damage or dehydration.

20:1

25
Q

Calculate the creatinine clearance, list the reference intervals for both males and females. Emphasize why the creatinine clearance is a good indicator of kidney function.

A 
Clearance  =  U x V / P
U  =	urine creatinine conc. (mg/dL)
V  =	urine volume (mL/min)
P  =	Plasma creatinine conc. (mg/dL)

Men: 107 – 120 mL/min
Women: 87 – 107 mL/min

26
Q

Fanconi Syndrome

Macroscopic
Microscopic

A

Macroscopically-Elevated Protein, Elevated Glucose, normal serum glucose

Microscopically-cystine crystals

27
Q

List the common findings with fanconi syndrome

A

Most common disorder associated is tubular dysfunction.

Generalized failure of tubular reabsorption in the proximal convoluted tubule.

28
Q

Cystinosis

Pathogenesis
Symptoms/Treatment
Urinalysis

A

Pathogenesis: intracellular deposition of cystine.

Symptoms/Treatment: Patients are unable to concentrate or acidify urine, results in growth retardation, rickets, acidosis, polydipsia, and polyuria. Patients must undergo dialysis or transplant.

Urinalysis: Hematuria, proteinuria, increased RBCs and cystine crystals.

29
Q

Cystinuria

Pathogenesis
Urinalysis

A

Pathogenesis: Inability of the renal tubules to reabsorb cystine filtered by the glomerulus.

Urinalysis: Hematuria, proteinuria, increased RBCs and cystine crystals.

30
Q

Cystinosis

Pathogenesis
Symptoms/Treatment
Urinalysis

A

Pathogenesis: Genuine inborn error of metabolism. Fanconi’s syndrome occurs

Symptoms/Treatment: In severe cases, gradual progression to renal failure.

Urinalysis: polyuria, generalized aminoaciduria and lack of urinary concentration.

31
Q

Homocystinuria

Pathogenesis
Symptoms/Treatment
Urinalysis

A

Pathogenesis: Defects in homocystine metabolism.

Symptoms/Treatment: In severe cases, gradual progression to renal failure.

Urinalysis: Gives a positive cyanide-nitroprusside test. Must be confirmed with silver-nitroprusside test in which only homocystine reacts.

32
Q

Osmolarity

A

Can be determined by measuring the colligative properties of the solution and comparing this value with the value obtained from the pure solvent. Major uses of osmolarity includes includes renal concentrating ability, monitoring the course of renal disease, monitoring fluid and electrolyte therapy.

Normal serum 275-300 mOsm.
Normal urine 50-1400 mOsm.

33
Q

Free Water Clearance

A

The free water clearance is determined by first calculating the osmolar clearance using the standard clearance formula of COSM = (Uosm x V) / Posm and then subtracting the osmolar clearance value from the urine volume in mL/minute. Calculation of the osmolar clearance tells how much water must be clear each minute

34
Q

Specific gravity

A

Depends on the # of particles present in a solution and the density of these particles.

When evaluating renal concentrating ability, the substances of interest are small molecules, primarily sodium and chloride, but urea influences the specific gravity more than sodium or chloride.

35
Q

Acute Tubular Necrosis

Pathogensis
Urinalysis

A

Pathogenesis: Primary disorder associated with damage to the renal tubules. Caused by shock, trauma, and surgical procedures. Variable disease course.

Urinalysis: Urinalysis findings include mild proteinuria, microsocopic hemaoturia, and presence of renal tubular epithelial cells and casts, and other casts including hyaline, granular, waxy and broad.

36
Q

Renal tubular acidosis

Pathogenesis:

A

Pathogenesis: Due to inability to secrete adequate hydrogen ions, patients are unable to acidify urine, Inherited autosomal dominant trait.

37
Q

Diabetes Mellitus

Macroscopically
Microscopically

A

Macroscopically-Elevated glucose and ketones

Microscopically-unremarkable.

Proteins, glucose, ketones

38
Q

Discuss other carbohydrates that maybe elevated in the urine. Indicate the significance of elevated galactose

A

Presence of galactosuria indicating the inability to properly metabolize galactose to glucose. Laboratory testing involves detection of non-glucose related reducing substances.

39
Q

Compare and contrast type 1 diabetes mellitus and type 2 diabetes mellitus.

A

Type 1 usually present before the age of 40 the unset is usually sudden. The glucose is elevated because of a lack of insulin production.

Type 2 diabetes presents after the age of 40 is usually a slow on set and is often the result of obesity.

40
Q

Explain the role of the kidney in acid base balance

A

Homeostasis: Regulate Acid-Base Balance by maintaining blood pH at normal values (7.35-7.45).

Acidotic Conditions: H+ ions are secreted in exchange for sodium and bicarbonate ions.

Alkalotic Conditions: H+ ion secretion minimized, additional alkali ions are secreted.

41
Q

Erythropoietin

A

Hormone produced by the kidneys in response to tissue hypoxia to stimulate the production of RBCs thereby increasing amount of oxygen carried to the tissues

42
Q

Prostaglandin

A

Hormone produced by the renal medulla, increases the renal blood flow and the excretion of salt and water

43
Q

Renin

A

Ultimately stimulates the production of aldosterone, which regulates sodium and potassium and water secretion.

44
Q

Angiotensin II

A

A vasoconstrictor that reduces the glomerular filtration rate and stimulates the production and release of aldosterone

45
Q

Aldosterone

A

Basic function is to stimulate the kidneys to retain or secrete sodium and potassium ions. When total blood volume is decreased, sodium and water are retained, if serum potassium is elevated, more potassium is excreted which in turn increases arterial pressure

46
Q

ADH: (Antidiuretic hormone)

A

ADH (vasopressin) alters the permeability of the distal tubule and collecting duct.
When blood volume is decreased, ADH secreted which causes an increase in water reabsorption and when blood volume is increased, ADH secretion is inhibited, more water is excreted.

47
Q

Discuss the renin-angiotensin-aldosterone system

A

When the juxtaglomerular apparatus senses change it activates the rennin-angiotensin-aldosterone system. Renin, which is produced by the juxtaglomerular apparatus, is secreted and reacts with the bloodborne substrate angiotensiongen to produce angiotensin I. As angiotensin I passes through the lungs it is converted to angiotensin II.

48
Q

Nephrolithiasis

A

Disease process involving the formation of stones, most common is calcium mixed with oxalate or phosphate. Involves changes in urine pH, increased urine stasis, presence of foreign body deposits in urinary tract.

49
Q

Phenylketonuria

A

Caused by a failure to inherit the gene to produce phylalanine hydroxylase. Most common is aminoacidurias. Initially diagnosed with a blood test shortly after birth. Urine test is used a screening test to ensure proper dietary intake

50
Q

Alkapturia

A

Occurs from the failure to inherit the gene to produce the enzyme homogentisic acid oxidase. Without the enzyme, homogentisic acid accumulate in the blood, tissues, and urine. Urine darkens upon standing.

51
Q

MSUD: Maple Sugar Urine Disease

A

Caused by an inborn error of metabolism. Failure to inherit the gene for the enzyme necessary to produce oxidative decarboxylation of these keto acids result in the accumulation of ketoacids. Most frequent screening test for detection of keto acids is the 2,4 dinitrophenylhydrazine (DNPH) reaction. Adding DNPH to urine that contains ketoacids will produce a yellow turbidity or precipitate

52
Q

Melanuria

A

Increased production of melanin leads to a darkening of urine. Elevation of urinary melanin is a serious finding that indicates the over proliferation of the normal melanin-producing, producing a malignant melanoma.

53
Q

Homocystinuria

A

Defects in homocystine metabolism. Gives a positive cyanide-nitroprusside test. Must be confirmed with silver-nitroprusside test in which only homocystine reacts.

Urinalysis (3 decks)

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