Kidney Function Flashcards
Acute Glomerulonephritis
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.
Discuss the pathogenesis of this condition and the projected outlook for the patient.
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.
Discuss the anatomy and physiology of the glomerulus.
The glomerulus consists of a coil of approximately eight capillary lobes known as the capillary tuft that is housed within the Bowman’s capsule.
Rapid Progressive glomerulonephritis(RPGN) crescentic glomerulonephritis
Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests
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
Membaranous glomerulonephritis(MGM)
Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests
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
Membranoproliferative glomerulonephritis(MPGN)
Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests
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
Chronic Glomerulonephritis
Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests
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.
IgA nephropathy
Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests
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
Focal segmented glomerulosclerosis(FSGS)
Pathogenesis
Glomerular Changes
Urinalysis
Chemistry Tests
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.
Pyelonephritis
Macroscopically
Microscopically
Macroscopically-cloudy urine, protein, blood, nitrites, leukocyte esterase
Microscopically-WBCs, renal epithelial cells, WBC casts, moderate bacteria
Proximal tubule
Mode of Reabsorption and Substance
Passive - H2O, Cl-, K+, urea
Active - Na+, HCO3-, glucose, proteins, phosphate, sulfate, Mg+, Ca2+, uric and amino acids
Loop of Henle
Mode of Reabsorption and Substance
Thin descending - Passive - H2O, urea
Loop of Henle - Passive - Na+, Cl-, urea
Thick ascending(medullary and cortical) - Passive - urea
Active - Na+, Cl-
Distal Tubule (convoluted portion)
Mode of Reabsorption and Substance
Passive - H2O
Collecting Tubules
Mode of Reabsorption and Substance
Cortical Passive - H2O, Cl-
Active - Na+
Medullary Passive - H2O, urea
Discuss where the ultrafiltrate components are secreted in the nephron.
Proximal Tubule
Loop of Henle
Distal Tubule
Collecting Tubules
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+
Acute Pyelonephritis
Physical and Chemical Examination
Microscopic Examination
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
Chronic Pyelonephritis
Physical and Chemical Examination
Microscopic Examination
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
Acute interstitial nephritis
Physical and Chemical Examination
Microscopic Examination
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
Cystitis
Physical and Chemical Examination
Microscopic exam
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
Nephrotic syndrome
Macroscopic and Microscopic
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,
Discuss the disease process of nephrotic syndrome
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
BUN
Definition and reference range
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
Creatinine
Definition and reference range
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
BUN creatinine ratio
Definition and reference range
The BUN creatinine ratio compares the two results and used to determine either acute kidney damage or dehydration.
20:1
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.
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
Fanconi Syndrome
Macroscopic
Microscopic
Macroscopically-Elevated Protein, Elevated Glucose, normal serum glucose
Microscopically-cystine crystals
List the common findings with fanconi syndrome
Most common disorder associated is tubular dysfunction.
Generalized failure of tubular reabsorption in the proximal convoluted tubule.
Cystinosis
Pathogenesis
Symptoms/Treatment
Urinalysis
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.
Cystinuria
Pathogenesis
Urinalysis
Pathogenesis: Inability of the renal tubules to reabsorb cystine filtered by the glomerulus.
Urinalysis: Hematuria, proteinuria, increased RBCs and cystine crystals.
Cystinosis
Pathogenesis
Symptoms/Treatment
Urinalysis
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.
Homocystinuria
Pathogenesis
Symptoms/Treatment
Urinalysis
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.
Osmolarity
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.
Free Water Clearance
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
Specific gravity
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.
Acute Tubular Necrosis
Pathogensis
Urinalysis
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.
Renal tubular acidosis
Pathogenesis:
Pathogenesis: Due to inability to secrete adequate hydrogen ions, patients are unable to acidify urine, Inherited autosomal dominant trait.
Diabetes Mellitus
Macroscopically
Microscopically
Macroscopically-Elevated glucose and ketones
Microscopically-unremarkable.
Proteins, glucose, ketones
Discuss other carbohydrates that maybe elevated in the urine. Indicate the significance of elevated galactose
Presence of galactosuria indicating the inability to properly metabolize galactose to glucose. Laboratory testing involves detection of non-glucose related reducing substances.
Compare and contrast type 1 diabetes mellitus and type 2 diabetes mellitus.
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.
Explain the role of the kidney in acid base balance
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.
Erythropoietin
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
Prostaglandin
Hormone produced by the renal medulla, increases the renal blood flow and the excretion of salt and water
Renin
Ultimately stimulates the production of aldosterone, which regulates sodium and potassium and water secretion.
Angiotensin II
A vasoconstrictor that reduces the glomerular filtration rate and stimulates the production and release of aldosterone
Aldosterone
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
ADH: (Antidiuretic hormone)
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.
Discuss the renin-angiotensin-aldosterone system
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.
Nephrolithiasis
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.
Phenylketonuria
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
Alkapturia
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.
MSUD: Maple Sugar Urine Disease
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
Melanuria
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.
Homocystinuria
Defects in homocystine metabolism. Gives a positive cyanide-nitroprusside test. Must be confirmed with silver-nitroprusside test in which only homocystine reacts.
