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304 Cards in this Set
- Front
- Back
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what are most glomerular diseases caused by?
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- immunologically mediated
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what are most tubular and interstitial diseases mediated by?
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- toxic or infectious agents
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when do you see prerenal azotemia?
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- hypoperfusion of kidneys:
- hemorrhage - shock - volume deplition - CHF |
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when do you see postrenal azotemia?
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- urine flow is obstructed below level of kidney
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define uremia
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- when azotemia becomes associated with clinical signs
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what can there be secondary involvement of with uremia?
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- GI system: uremic gastroenteritis
- peripheral nerves: peripheral neuropathy - heart: uremic fibrinous pericarditis |
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what is acute renal failure?
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- reduced or no urine flow (oliguria or anuria)
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what clincal symptoms do you see in renal tubular defects?
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- polyuria
- nocturia - electrolyte disorders (met acidosis) |
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describe the four stages of chronic renal failure
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1. diminished renal reserve
2. renal insufficiency 3. renal failure 4. end-stage renal disease |
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define: diminisehd renal reserve
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- GFR is 50% normal
- BUN and creatinine are normla - asymptomatic - more susceptible to developing azotemia with additional renal insult |
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define: renal insufficiency
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- GFR is 20-50% nromal
- azotemia appears, usually associated with anemia and hypertension. polyuria and nocturia cna occur as a result of decreased concentration ability - sudden stress can precipitate uremia |
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what may happen over time with a patient who's only got one kidney?
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- progressive glomerular sclerosis in the remaining kidney as a result of adaptive changes in hypertophied nephrrons
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why are ectopic kidneys predisposed to infection and obstruction to urinary flow?
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- kinks in the ureters due to abnormal location
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which genes are involved in polycystic kidney disease?
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- chr 16: PKD1 -> polycystin-1
- chr 4: PKD2 -> polycystin-2 |
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how do you explain both lung and kidney disease in Goodpasture syndrome?
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- anti-GBM antibodies cross react with other BMs, esp in the lung alveoli
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which antigens can cause circulating immune complex nephritis (not specific for the glomerulus)
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- streptococci
- Hep B (HBsAg) - Hep C - treponema pallidum - plasmodium falciparum` |
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what causes focal segmental glomerulosclerosis?
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- adaptive change in the relatively unaffected glomeruli of diseased kidneys (think of agenic kidneys- same principle)
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what is the prevalence of unilateral agenesis?
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- relatively common (1 in 1000 births)
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how does unilateral renal agenesis present?
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- either completely asymptomatic
- or, seen with other congenital anomalies - a single umbilical artery may clue you in to the diagnosis |
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what causes unilateral renal agenesis?
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- failure of the uretic buds to develop
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what happens with complete divison of a ureteric bud?
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- bifid ureter with a double kidney on one side
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what happens with crossed renal ectopia?
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- fused kidneys on one side
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what happens with double uretic buds?
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- supernumerary kidney
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what happens with incomplete division of a ureteric bud?
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- bifid ureter with a partially divided kidney
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what does the ureteric bud give rise to?
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- ureter
- renal pelvis - major and minor clayces - 1-3 million collecting tubules |
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describe the Potter sequence
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- anuria, oligohydramnios and hypoplastic lungs secondary to the oligohydramnios
- in 85% of the cases, other severe defects (absence or abnormalities of the vagina and uterus, vas deferens , and seminal vessels) are seen |
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what can fibromuscular dysplasia (FMD) cause?
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- can lead to bilateral renal artery stenosis (beaded appearance on angiography)
- mediated by an autoimmune response - a type of vasculitis |
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define: angiography
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The use of X-ray images of blood vessels after injecting dye (contrast material) into the bloodstream. Used as a tool to diagnose many diseases affecting the arteries and veins, including inflammatory diseases.
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how do you treat renal stenosis caused by fibromuscular dysplasia?
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- renal artery balloon angioplasty
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what is the incidence of unilateral renal artery stenosis?
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- relatively uncommon cause of hypertension
- responsible for 2-5% of cases of hypertension |
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how do you treat renal artery stensis?
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- surgical treatment
- successful in 70-80% of patients |
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what happens with unilateral renal artery stenosis?
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- hypertension that is equal in magnitude to the degree of stenosis
- initially, due to the increase in renin secretion |
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what is the most common cause of renal artery stenosis?
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- in 70% of cases, is atheromatous plaque at the origin of the renal artery
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what is the epidemiology of renal artery stenosis caused by artheromatous plaque?
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- more frequent in men
- increases with age, and diabetes |
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what is the second most common cause of renal artery stenosis?
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- fibromuscular dysplasia of the renal artery
- thickening of either the intima, media, or adventitia of the artery |
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what are the subclassifications of fibromuscular dysplasia?
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1. intimal medial hyperplasia
2. adventitial hyperplasia |
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what is the epidemiology of fibromuscular dysplasia?
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- more common in women
- tend to occur in younger age groups (30s-40s) |
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describe the progression of kidney ischemia
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- ischemic kidney is reduced in size, and shows diffuse atropy
- the arterioles of the ischemic kidney are protected from the affects of high BP -> show only mild ateriolosclerosis - the contralateral nonischemic kidney may have MORE SEVERE arteriolosclerosis |
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what causes double ureters?
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- usually from double or split ureteral bud
- may have separate courses to the bladder, but usuaully drain through a single uretheral orifice - usually have no clinical significance |
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what is a ureteropelvic junction obstruction?
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- congenital disorder
- results in hydronephrosis - usually presents in children - more common in boys |
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why doesn't Angiotensin II decrease GFR since it causes peripheral vasoconstriction?
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- Ang II also vasoconstricts the efferent arteriole -> maintains GFR even with reduced plasma flow
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what happens to pH levels with renal artery stenosis?
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- pH rises -> metabolic alkalosis due to increased net acid SECRETION from hyperaldosteronism
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what happens to K with renal artery stenosis?
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- K SECRETION increases due to increased levels of aldosterone
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which part of the urinary system is involved if you see white cell casts in the urine?
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- the kidneys
- leukocytes are compressed together in the renal tubules |
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where is the involvement if you see red blood cell casts?
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- kidney
- compression of RBCs in the renal tubules |
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what are you concerned about when you see a UTI in a pregnant woman?
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- spread to the uterus
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what is a normal range for blood pH?
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7.35-7.45
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what are normal values for PCO2?
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33-45 mmHg
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what are normal values for PO2?
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75-105 mmHg
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what are normal fasting glucose levels in serum?
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- 70-110 mg/dL
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what are normal post-prandial serum glucose levels?
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2 hours postprandial: <120mg/dL
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what are normal plasma bicarb levels?
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22-28 mEq/L
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when do you get mixed acidosis?
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- cardiopulmonary arrest
- have some lactic acidosis (metabolic) - respiratory acidosis from ventilary standstill |
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what defines a metabolic acidosis?
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- plasma pH and HCO3- are low
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what defines a respiratory acidosis?
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- plasma pH is low
- arterial CO2 is high |
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how do you calculate the volume of a fluid compartment?
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- volume = (quantity of stuff administered)/(concentration of indicator in compartment)
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where do you find p-ANCA?
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sometimes seen in Goodpasture's syndrome patients
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what causes Goodpasture Syndrome?
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- autoantibodies against the noncollagenous domain of the a-3 chain of collagen 4
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what is the epidemiology of Goodpasture Syndrome?
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- occur in the teens and twenties
- more prevalent in MEN (in contrast to the other autoimmune diseases) |
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where do you see involvement for Goodpasture syndrome?
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- inflammatory destruction of basement membrane in:
- kidney glomeruli - lung alveoli - gives rise to proliferative, rapidly progressing glomerulonephritis - necrotizing hemorrhagic interstitial pneumonitis |
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what can trigger Goodpasture syndrome?
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- environmental insult: virla infection, exposure to hydrocarbon solvens, smoking to unmask the cryptic epitose
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what is the HLA association with Goodpasture Syndrome?
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- HLA-DRB1*1501 and *1502
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what do you see on histology in the lungs for Goodpasture syndrome?
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- lungs are heavy with red-brown consolidation
- alveoli contain hemosiderin-laden macrophages - lnear deposits of Ig along the BM of the septal walls |
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what do you see on histology in the kidneys for Goodpasture syndrome?
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- focal proliferative glomerulonephritis
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how does Goodpasture syndrome initially present? how do patients die?
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- respiratory symptoms: hemoptysis
- focal pulmonary consolidations on X-ray - most common cause of death: uremia |
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the ureter lies immediately anterior to which antatomical structure?
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- the external iliac artery
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where is the origin of the common iliac artery?
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- bifurcation of the abdominal aorta
- occurs at the level of the 4th lumbar vertebra |
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where is the origin of the internal iliac artery?
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- at the bifurcation of the common iliac artery (occurs at the level of the first sacral vertebra)
- the ureter and internal iliac artery both enter the pelvis, with the ureter on the lateral side of the artery |
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where is the origin of the gonadal artery?
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- abdominal aorta, usually between the renal artery and the inferior mesenteric artery
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what tumor has dense immature islands of epithelial cells, spindled fibrolast-like stromal cells, and poorly formed tubular structures?
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Wilms tumor
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describe a Wilms' tumor
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- neoplasm of the embryonic renal blastema
- has both neoplastic epithelial and stromal components - have recognizable glomerular and/or tubular strucutres |
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describe a rhabdomyosarcoma
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- cytoplasmic content of eosinophilic muscle proteins (thick and thin filaments)
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describe a Ewing's sarcoma
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- monotonous ball of primitive, small round cells with a thin rim of clear cytoplasm
- a tumor of bone |
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describe the clinical presentation of Hodgkin's disease
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- lymphoid maligancy
- presents with lymphadenopathy of cervical and mediastinal nodes - see inflammatory cells and Ree-Sternberg cells |
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how does a neuroblastoma present?
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- frequently presents as an abdominal mass in children
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are skeletal muscle neoplasms most often maligant of benign?
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- malignant
- exception: cardiac rhabdomyoma |
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describe the epidemiology of rhabdomyosarcoma
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- most common soft tissue sarcoma of childhood and adolescence
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what are the classifications for rhabdomyosarcoma?
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1. embryonal
2. alveolar 3. pleomorphic |
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describe the histology of rhabdomyosarcoma
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- eccentric eosinophilic granular cytoplasm
- thick and thin filaments - the cells can be round or elongated (tadpole or stap cells) |
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what is the most common type of rhabdomyosarcoma?
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- embryonal (66%)
- variants: sarcoma botryoides, and spindle cell |
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describe embryonal rhabdomyosarcoma
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- occurs in children under 10
- sheets of both malignant round and spindled cells in variably myxoid stroma |
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describe alveolar rhabdomyosarcoma
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- common in mid-adolescence
- found in deep musculature of extremities - on histology, the fibrous septae that divide cells into clusters looks like pulmonary alveoli |
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describe pleomorphic rhabdomyosarcoma
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- rare
- found in deep soft tissue of adults |
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what is Ewing Sarcoma?
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- aka primitive neuroectodermal tumor (PNET)
- malignant small round cell tumor of bone and soft tissue - hard to differentiate from lymphoma, rhabdomyosarcoma, neuroblastoma and oat cell carcinoma |
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what is the epidemiology of Ewing Sarcoma and PNET?
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- predilection for whites
- blacks are almost never affected |
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describe the morphology of Ewing Sarcoma and PNET
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- invade the cortex and periosteum -> soft tissue mass
- sheets of uniform small, round cells - usually arises in the diaphyses of long tubular bones (femur and flat bones of pelvis) |
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how do Ewing Sarcoma and PNET present?
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- painful enlarging masses
- tender, warm and swollen |
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what is a congenital disorder that results in hydronephrosis?
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- ureteropelvic junction obstruction
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describe ureteropelvic junction obstruction
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- presents in infants or children
- more common in boys - in adults, the obstruction is more common in females - there is agenesis of the kidney on the opposite side in a significant number of cases, possibly resulting from obstructive lesions in utero |
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what are the most common causes of UTI, in descending order?
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1. E. coli
2. Proteus 3. Klebsiella 4. Enterobacter |
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what are the two ways in which bacteria can reach the kidneys?
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- hematogenous infection: through the blood stream (less common in causing pyelonephritis)
- ascending infection: through the lower urinary tract |
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describe how hematogenous infection leading to pyelonephritis may occur
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- seeding of kidneys from septicemia or infective endocarditis
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how do you distinguish pre-renal failure from acute tubular necrosis?
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- ADH is high in prerenal failure -> urea, water, and sodium resorption
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what is the fractional sodium excretion in acute tubular necrosis and pre-renal failure?
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- prerenal failure: Na excretion is <1%
- acute tubular necrosis: >2% |
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what is the normal ratio of BUN:creatinine?
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- 12-20
- higher ratios are seen in prerenal azotemia - lower ratios are seen in acute tubular necrosis |
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what are urinary sodium levels in prerenal failure?
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- <20 mEq/L
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what are urinary sodium levels in acute tubular necrosis?
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- >40 mEq/L
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what is urine osmolality in prerenal failure?
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> 500mOsml/kg
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what is urine osmolality in acute tubular necrosis?
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< 350 mOsmol/kg
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what is urine/serum creatinine in prerenal failure?
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> 40
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what is urine/serum creatinine in acute tubular necrosis?
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<20
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what are the signs of bladder instability?
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elderly woman presents with urinary urgency and incontinence
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oxybutynin
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- direct antispasmodic effect
- inhibits muscarinic action of ACh on smooth muscle - used for bladder instability - has 1/5 the anticholinergic activity of atropine, but 4-10 x the antispasmodic activity |
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bethanechol
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- choline-like compound that stimulates muscarinic receptors - can cause contraction of detrusor muscle
- indicated for treatment of urinary retention |
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bumetanide
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- loop diuretic
- used to treat edema |
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metoprolol
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- b1 selective antagonist
- used for hypertension and tachyarrhythmias |
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what two drugs do you not want to give with diabetes?
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- metoprolol and glyburide
- metoprolol can mask hypoglycemia |
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neostigmine
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- inhibits acetylcholine hydrolysis in synaptic cleft via ACh-esterase inhibition
- can cause detrusor muscle contraction - used to treat urinary retention |
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lomefloxacin
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- fluoroqunolone antibiotic for treatment of both gram-negative and gram positive bugs
- primarily used lower respiratory tract infections and UTIs |
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which drugs have been associated with arthropathy, myalgias, and leg cramps when given to children?
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- lomefloxacin
- fluoroquinolone |
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azithromycin side effects
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- macrolide antibiotic that is generally well tolerated
- mild nausea and abdominal pain |
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metronidazole side effects
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- antiprotozoal and antibacterial
- convulsive seizures - peripheral neuropathy - can produce disulfiram like reactions when taken with alcohol |
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rifampin side effets
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- used for TB and asymptomatic carriers of Neisseria meningitidis
- hepatotoxicity, hyperbilirubinemia, porphyria, cancer |
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tetracycline side effects
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- antibiotic
- photosensitivity - pseudotumor cerebri - maculopapular rashes |
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what is derived from the ureteric bud?
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- collecting system:
- collecting ducts - minor and major calyces - renal pelvis |
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what is derived from the metanephric mesoderm?
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- ascending loop of Henle
- Bowman's capsule - descendign loop of Henle - glomerular tuft |
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what is a dangerous complication of a dissecting aortic aneurysm?
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- bilateral renal infarction
- the dissecting aneurysm occludes both renal arteries -> bilateral renal infarction with flank pain and hematura |
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what can sickle cell crisis do to the kidneys?
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- can cause papillary necrosis with hematuria
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how do diuretics lead to aldosterone excess and hypokalemia? (method 1)
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1. volume depletion stimulates aldosterone creation -> stimulates K excretion
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how do diuretics lead to aldosterone excess and hypokalemia? (method 2)
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2. saline diuresis increases saline delivery to CT -> increased Na along with elevated aldosterone promotes Na reabsorption in the CD -> raises luminal negativity -> promotes secretion of cations (esp. H) -> raises bicarb reabsorption
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how do diuretics lead to aldosterone excess and hypokalemia? (method 3)
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3. saline diuresis causes rapid fluid flow into the DT -> keeps luminal potassium concnetration low by carrying it away -> prevents accumulation of K that enters the lumen -> crease steep concetration gradient for additional K loss in the urine
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what is the most common cause of metabolic alkalosis?
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- thiazide or loop diuretics
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which part of the renal vasculature is most vulnerable during a sickle cell crisis?
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- vasa recta
- the high osmolarity of the renal medualla particularly favors sickling of erythrocytes - can cause patchy papillary necrosis, proteinuria, and sometimes cortical scarring |
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what can sickling crises be triggered by?
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- hypoxia from high altitude or pneumonia
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why aren't glomerular capillaries involved during sickle cell crises?
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- are small enough to be occluded, but are well oxygenated enough and the blood within them is not hypertonic
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pseudomonas aeruginosa
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- gram neg rol
- oxidase positive, lactose neg - opportunistic - increase chance in causing UTIs in patients with indwelling catheters or who are on antibiotics |
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candida albicans
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- yeast that can cause UTIs in poorly controlled diabetics b/c glucose in urine enhances growth
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enterococcus faecalis
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- gram + coccus
- causes UTIs in elderly men with prostate problems |
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E coli
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- lactose positive
- oxidase negative - gram neg rod - common cause of UTIs |
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Klebsiella pneumoniae
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- lactose positive
- oxidase neg - gram neg rod - causes UTIs in poorly controlled diabetics b/c glucose in urine enhances its growth |
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Proteus mirabilis
|
- gram neg rod
- member of the enterobacteriacaea family - lactose neg - contains urease -> splits urea to give ammonia -> raises pH of urine |
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which organisms are more likely to thrive if there are stones in the bladder?
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- proteus mirabilis
- can hid in the stones and cause UTIs - predisposes the development of stones |
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staphlococcus saprophyticus
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- catalase positive
- coagulase neg - gram positive coccus - causes UTIs in young women |
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what are staghorn calculi associated wtih?
|
- magnesium ammonum phosphate stones
- caused by urea-splitting bacteria (e.g. proteus) - more common in women then men - more common in patients with indwelling chronic bladder catheterization |
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what is a common infection in patients with an indwelling bladder catheter?
|
- magnesium ammonium phosphate stones (with staghorn calculi) from urea-splitting bacteria
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where are calcium-containing stones most frequently seen?
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- in patients with hypercalcinuria WITHOUT hypercalcemia
- 1/5 of patients with calcium stones have hyperuricosuria |
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how do staghorn caliculi form?
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- recurrent proteus infection
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what are staghorn stones made out of?
|
- progresive accumulation of struvite or magnesium ammonium phosphate
- ammonium comes from the hydrolysis of urea (Proteus, and some strains of Staphlococcus) |
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what is the most common metabolic anomaly associated with urinary stones made of calcium phosphate or calcium oxalate?
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- idiopathic hypercalcuria
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what sort of stones can strict vegetarianism cause?
|
- increase oxaluria and formation of oxalate stones
|
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what are normal sodium levels in the blood?
|
135-145 mEq/L
|
|
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what are normal chloride levels in the blood?
|
95-105 mEq/L
|
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what are normal potassium levels in the blood?
|
3.5-5.0 mEq/L
|
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what are normal bicarbonate levels in the blood?
|
22-28 mEq/L
|
|
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what are normal magnesium levels in the blood?
|
1.5-2.0 mEq/L
|
|
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when is adequate replenishment of water loss by excretion interfered with?
|
- surgury
- can cause severe dehydration -> fever, psychic disturbances, death |
|
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what are symptoms of dehydration?
|
Initially, one experiences thirst and discomfort, possibly along with loss of appetite and dry skin. This can be followed by constipation. Athletes may suffer a loss of performance of up to 50%, and experience flushing, low endurance, rapid heart rates, elevated body temperatures, and rapid onset of fatigue.
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what is a 'finely granular' kidney surface indicative of?
|
- presence of arteriolonephroscloerosis (benign nephrosclerosis)
- caused by benign hypertension |
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descibe the vascular pathologies of hypertension
|
- accelerates atherogenesis
- causes degernative changes to large and medium arteries -> aortic dissection and cerebrovascular hemorrhage - associated with 2 forms of small vessel disease: 1. hyaline arteriolosclerosis 2. hyperplastic arteriolosclerosis |
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what are the two forms of small vessel disease that are caused by hypertension?
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1. hyaline arteriolosclerosis
2. hyperplastic arteriolosclerosis |
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describe hyaline arteriolosclerosis
|
- arteriolar wall is hyalinized
- lumen is narrowed |
|
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describe hyperplastic arteriolosclerosis
|
- onionskinning
- causes luminal obliteration - secondary ischemic changes - see wrinking of glomerular capillary vessels |
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who gets hyaline arteriolosclerosis?
|
- elderly patients, with or without hypertension
- more generalized and more sever in patients with hypertension - also common in diabetes |
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what do you see in benign bnephrosclerosis?
|
- hyaline arteriolosclerosis
- arteriolar narrowing causes diffuse impairment of renal blood supply -> loss of nephrons, and symmetric contraction of kidneys |
|
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when do you get hyperplastic arteriolosclerosis?
|
- seen in acute or severe elevations of blood pressure (e.g. malignant hypertension)
|
|
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what is the appearance of hyperplastic arteriolosclerosis?
|
- onionskin, concentric, laminated thickening of the walls
- progressive narrowing of the lumina |
|
|
what vascular change do you see in malignant hypetension?
|
- hyperplastic arteriolosclerosis
- in addition to the hyperplastic changes seen in the vessels, will also get deposits of fibrinoid and acute necorsis of the vessel walls -> necrotizing arteriolitis |
|
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what is necrotizing arteriolitis?
|
- deposition of fibrin and acute necrosis of blood vessel walls seen in hyperplastic arteriolosclerosis with malignant hypertension
|
|
|
why do you get a finely granular surface on a kidney?
|
- systemic benign hypertension leads to arteriolonephrosclerosis
- arises from multifocal loss of glomeruli in teh superficial cortex -> gives rise to puckered appearance - caused by chronic ischemia from stenosis of small arteries and arterioles - can also be caused by diabetes |
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what does acute hypovolemic shock lead to?
|
- acute tubular necrosis
- due to sudden drop in perfusion |
|
|
describe acute tubular necrosis
|
- epithelial tubular cells undergo ischemic necrosis and detach from the BM
- rapid decrease in GFR -> acute renal failure - on autopsy, kidneys look large and edematous |
|
|
how do the kidneys look after acute hypovolemic shock?
|
- on autopsy, look large and edematous
|
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how do kidneys look at end stage kidney failure?
|
- look atrophic and shrunken
- cortex has disappeared and frequently shows cysts (esp if patient has been on dialysis) |
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how do kidneys look after malignant hypertension?
|
- can cause renal failure after severe arteriolar damage from hyperplastic arteriolosclerosis -> necrotizing arteriolitis
- kidney will have mottled, hemorrhagic appearance |
|
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what can happen to kidneys if you have subacute infective endocarditis?
|
- septic emboli -> wedge- shaped areas of necrosis
|
|
|
what has many overlapping features with IgA nephropathy?
|
- Henoch-Schonlein purpura
|
|
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what is IgA nephropathy also known as?
|
- Berger disease
|
|
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what is Berger disease also known as?
|
- IgA nephropathy
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|
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what causes secondary IgA nephropathy?
|
- liver and intestinal diseases
|
|
|
- how do you diagnose IgA nephropathy?
|
- look for prominnet IgA deposits in the mesangial regions
|
|
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what do you see on histology for IgA nephropathy?
|
- mesangial deposition of IgA
- often with C3 and PROPERDIN - lesser amounts of IgG or IgM |
|
|
what is the clincial presentation of IgA nephropathy?
|
- recurrent gross of microscopic hematuria
- hematuria subsides, but returns every few months - follows infection of respiratory or GI tract - slow progression to renal failure in 15-40% of cases |
|
|
what triggers IgA neprhopathy?
|
- respiratory or GI infection
- a genetic or acquired abnormality of immune regulation causes increased mucosal IgA synthesis after exposure to environmental antigens |
|
|
what is the main immunoglobulin in mucosal secretions?
|
- IgA
|
|
|
describe the mechanism of IgA nephropathy
|
- entrapment of IgA immune complexes in the mesangium
- presence of C3 and the absence of C1q and C4 indicates activation of the alternative complement pathway |
|
|
which disease are seen with increased frequency with IgA nephropathy?
|
- gluten enteropathy (celiac disease)
- liver disease |
|
|
what causes glomerular crescent formation?
|
- proliferation of epithelial cells and infiltration of monocyte-macrophages
|
|
|
what do glomerular crescents suggest?
|
- rapidly progressive glomerulonephritis
|
|
|
what does podocyte foot process effacement suggest?
|
- when seen as the only finding, suggests minimal change disease -> major cause of nephrotic syndrome in children
|
|
|
what does subendothelial electron-dense deposits suggest?
|
- 'humps'
- poststreptococcal glomerulonephritis - immunofluorescence for IgG, IgM, and C3 yields a granular pattern - should also see decreased complement levels in serum |
|
|
what does thickening of the walls of glomerular capillaries suggest?
|
- tram-tracking -> membranoproliferative glomerulonephritis
|
|
|
what is another name for minimal change disease?
|
- lipoid nephrosis
|
|
|
what are dense deposits indicative of?
|
- type II membranoproliferative glomerulonephritis
|
|
|
how do you differentiate type I and II membranoproliferative glomerulonephritis?
|
- type I MPGN: subendothelial electron-dense deposits
- type II MPGN: dense-deposit disease |
|
|
what are mesangial deposits indicative of?
|
- IgA nephropathy
|
|
|
what are subendothelial deposits indicative of?
|
- type I membranoproliferative glomerulonephritis
|
|
|
what are subendothelial spikes indicative of?
|
- membranous glomerulonephritis
|
|
|
what is the most common cause of nephrotic syndrome in aduts?
|
- membranous glomerulopathy: a form of immune complex disease
|
|
|
how do you describe membranous glomerulopathy?
|
- aka mebranous nephropathy
- diffuse thickening of the glomerular capillary wall - accumulation of deposits along the subepithelial side of the BM |
|
|
what causes secondary membranous nephropathy?
|
- drugs
- underlying malignang tumors - SLE - infections - other autoimmune disorders |
|
|
what drugs can cause membranous nephropathy?
|
- penicillamine
- captopril - gold - NSAIDs |
|
|
what sort of kidney problems are caused by NSAIDs?
|
- membranous nephropathy
- minimal change disease |
|
|
what types of tumors can cause membranous nephropathy?
|
- carcinoma of the lung and colon
- melanoma |
|
|
what types of infections can cause memrbanous nephropathy?
|
- chronic hep B, hep C, syphilis, schistosomiasis, malaria
|
|
|
what autoimmune diseases can cause membranous nephropathy?
|
- SLE
- thyroiditis |
|
|
what do you see on histology for membranous glomerulopathy?
|
- uniform diffuse thickening of the glomerular capillary wall
- irregular spikes protruding from the GBM |
|
|
what is another name for a Wilms tumor?
|
- nephroblastoma
|
|
|
how do cortical adenomas present?
|
- small (under 2 cm) benign tumors found on autopsy
|
|
|
what is a oncocytoma?
|
- epithelial tumor made of large, EOSINOPHILIC cells
- arises from intercalated cells of the collecting ducts |
|
|
where do renal adenomas come from?
|
- renal tubular epithelium
- commonly found on autopsy |
|
|
what is another name for renal adenomas?
|
- papillary adenomas
|
|
|
define: hamartoma
|
A benign tumour made up of mature cells normally found in the region.
|
|
|
which of the benign tumors may cause clinical problems?
|
- oncocytomas- can get large -> up to 12 cm
- however, DO NOT USUALLY AFFECT YOUNG CHILDREN |
|
|
what causes Diabetes insipidus?
|
- most common cause: inadequate secretion of ADH (vasopressin)
'neurogenic DI' |
|
|
what causes addison's disease?
|
- failure of adrenal cortex to produce adrenocortical hormones
- lack of aldosterone -> decreased sodium reabsorption -> |
|
|
what are the functions of aldosterone?
|
1. Acting on mineralocorticoid receptors (MR) on principal cells in the distal convoluted tubule: increases the reabsorption of Na+ and H2O, and secretion of K+
2.also stimulates H+ secretion by intercalated cells |
|
|
what sort of pH problem can you get with overuse of diuretics?
|
- metabolic alkalosis
- diuretics increase excretion of Na and K -> decrease in plasma K levels |
|
|
when is tubular fluid isotonic?
|
- beginning of the proximal tubule
- end of the cortical collecting duct in the presence of ADH |
|
|
what sort of urine is a person making if she has a urine flow rate of 1ml/min?
|
- hypertonic urine
- has a significant amount of ADH present |
|
|
how do you calculate plasma osmolality?
|
(total body osmoles - urine osmoles)/(total body water - urine volume)
|
|
|
how do you calculate total body water?
|
- 60% of body weight
- NOT 2/3!!! |
|
|
what do linear deposits of IgG make you think of?
|
- Goodpasture syndrome
|
|
|
what are the two causes of rapidly progressive glomerulonephritis?
|
1. Goodpasture syndrome
2. idiopathic RPGN |
|
|
describe Goodpasture syndrome
|
- autoantibodies (IgG) directed against the basement membrane of glomeruli and alveoli -> rapidly progressive glomerulonephritis and pulmonary hemorrhage
|
|
|
what is the antigen of Goodpasture syndrome?
|
- peptide within the noncollagneous portion of the a3 chain of collagen type IV
|
|
|
what is the HLA association for Goodpastures syndrome?
|
- HLA-DRB1
|
|
|
what do you see on histology for Goodpastures syndrome?
|
1. crescents in glomeruli
2. linear deposits of immunoglobulin and complement |
|
|
what is the prognosis for Goodpastures?
|
- used to be really dismal
- death related to pulmonary hemorrahge or renal failure - now, prognosis is improved by use of plasma exchange |
|
|
what do you associate with electron dense subepithelial humps?
|
- poststreptococcal glomerulonephritis
|
|
|
what's Buerger's disease?
|
- a vasculitis that occurs in smokers
|
|
|
when do you see diffuse cortical necrosis?
|
- DIC, esp after overwhelming sepsis
- can also be seen after hypotension combined with vasoconstriction |
|
|
what can multiple myeloma do to the kidneys?
|
- renal deposition of amyloid protein and damage to both glomeruli and tubules
|
|
|
where does pyelonephritis usually affect?
|
- inflammation, most severe in the renal pelvis
|
|
|
where in the kidney does sickle cell anemia affect?
|
- usually the medulla most severely
- can cause papillary necrosis |
|
|
what are normal values for creatinine clearance?
|
men: 97-137 mL/min
women: 88-128 mL/min |
|
|
what are normal values for urine calcium?
|
100-300 mg/24 h
|
|
|
when can you use loop diuretics in relation to creatinine clearance?
|
- effective down to CrCl of 10mL/min
|
|
|
when can you use thiazide diuretics in relation to creatinine clearance?
|
- effective down to CrCl of 40mL/min
|
|
|
when can you use K sparing diuretics in relation to creatinine clearance?
|
- effective down to CrCl of 40mL/min
|
|
|
when do you use Furosemide?
|
- treatment of edema associated with CHF, hepatic cirrhosis, and renal disease
|
|
|
what is indapamide?
|
- thiazide diuretic
|
|
|
what is triamterine?
|
- K- sparing diuretic
|
|
|
what is fibroelastic hyperplasia?
|
- affects the MEDIA of larger interlobular and arcuate arteries
- caused by benign nephrosclerosis in hypertensive patients |
|
|
where is amyloid deposite in amyloidosis?
|
- deposition of amyloid material (homogeneous eosinophilic extracellular deposits) around small vessels
|
|
|
what do you see with E.coli enterotoxin?
|
- childhood hemolytic uremic syndrome with microangiopathic hemolytic anemia related to vascular intimal hyperplasia, fibrinoid necrosis, and thrombi
|
|
|
what is another word for lipoid nephrosis?
|
minimal change disease
|
|
|
where in the kidney does sickle cell disease affect?
|
- focal occlusions of the vasa recta (hypertonic, hypoxic envirnment of the renal medulla favors sickling)
- leads to patchy papillary necrosis, proteinuria, and sometimes cortical scarring |
|
|
which diuretic is contraindicated in renal failure?
|
- spironolactone (K sparing diruetic)
- you already have high K from crushed cells |
|
|
how do you get acute renal failure after being smushed?
|
- myoclobinuria of crush injury
|
|
|
what other abnormalities will you see with crush injury?
|
- hyperkalemia- since crushed cells release potassium
|
|
|
what is the effectiveness of acetazolamide limited by?
|
- presence of HCO3-
- alkalinization of urine using HCO3 aids in the treatment of myoglobinuria |
|
|
when is mannitol contraindicated?
|
- patients with anuria
|
|
|
where do potassium-sparing diuretics act?
|
- antagonists at the intracellular aldosterone receptor in the Collecting tubule
- dcrease expression of genes for sodium channels and the Na/K ATPase |
|
|
where do CA inhibitors act?
|
- at the proximal tubule
- inhibit Na bicarbonate reabsorption |
|
|
what is ethacrynic acid?
|
- a loop diuretic
- inhibits the Na/K/2Cl transporter in the ascending loop of Henle |
|
|
where do Thiazide diuretics act?
|
- inhibit the Na/Cl transporter in the early distal tubule
|
|
|
how does polycystic kidney disease present?
|
- hypertension secondary to renin production
- renal failure (elevated BUN and creatinine) - anemia (secondary to EPO production) |
|
|
what structures other than the kidney are affected in adult polycystic kidney disease?
|
- liver, pancreas, spleen, gonads
- berry aneurysms - abnormalities of cardiac valves |
|
|
what is the survival rate for Wilms tumor?
|
- 90% following surgery, chemo, and radiation
|
|
|
what can Wilms tumor cause regarding sexual development?
|
- gonadal dysgenesis
|
|
|
what do renal hamartomas cause?
|
- aka fibroma
- small, grey, benign nodule in the renal pyramids - usually only identified on autopsy - benign |
|
|
what are the normal values for BUN?
|
7-18 mg/dL
|
|
|
what are the normal values for serum creatinine?
|
0.6-1.2 mg/dL
|
|
|
what is the rate of creatinine production proportional to?
|
- muscle mass
- independent of renal function |
|
|
where does angiotensin II act on NaCl and water secretion?
|
- stimulates NaCl and water reabsoption in the PT
|
|
|
where is aldosterone synthesized?
|
- glomerulosa cells of the adrenal cortex
|
|
|
where does aldosterone act on NaCl and water secretion?
|
- TAL of henle's loop
- DT - CD |
|
|
what are aldosterone's effets on K?
|
- stimulates K secretion in the DT and CD
|
|
|
what two factors increase aldosterone secretion?
|
1. angiotensin II
2. increase in plasma [K] |
|
|
what are the three effects of ACE inhibitors?
|
1. decrease in NaCl and H2O reabsorption in the PT
2. decreased aldosterone -> decreased NaCl absorption in the TAL, DT, and CD; decreased K secretion 3. blocks angiotensin's vasoconstriction effects -> dilation of systemic arterioles |
|
|
what does angiotensin converting enzyme (ACE) degrade?
|
- bradykinin
- recall, kallikrein cleaves circulating kininogen to bradykinin, which is a vasodilator that acts by increasing release of NO and prostaglandins |
|
|
how does ANP regulate blood pressure?
|
1. Decrease TPR
2. increase urinary NaCl and water secretion |
|
|
what is urodilatin?
|
- almost the exact same as ANP, but differs by 4 amino acids
- secreted in the DT and CD - only made by the kidneys |
|
|
what causes a rise in urodilatin
|
- rise in BP and increase in the effective circulating volume
|
|
|
what is urodilatin's action?
|
- inhibits NaCl and water reabsorption across the medullary protion of the CD
|
|
|
what are the sympathetic nerves' effects on the kidney
|
- catecholamines secreted by sympathetic nerves (NE) and from the adrenal medulla (Epi) stimulate NaCl and water reabsorption by the PT, TAL, DT, and CD
|
|
|
where is dopamine secreted, and what does it do in the kidney?
|
- released from DA neurons in the kidneys
- opposite action of NE and Epi |
|
|
what is the main difference between ICF and plasma?
|
- plasma has more protein
|
|
|
how do you calculate total body water, ICF, and ECF from body weight?
|
total body water = 0.6 x BW
ICF = 0.4 x BW ECF = 0.2 x BW |
|
|
how do you roughly estimate ECF osmolality?
|
- 2x the plasma [Na]
|
|
|
what is a more accurate estimate of plasma osmolality?
|
plasma osmolality =
|
|
|
what do you administer if a patient's vascular volume needs to be increased?
|
- give something that can't be filtered out by the kidneys: 5% albumin solution
|
|
|
what do you administer if a patient's ECF is needed?
|
- give isotonic solution (0.9% NaCl)
|
|
|
what happens when a patient is hypoosmotic?
|
- water shifts into cells
- neuro changes: nausea, malaise, headache, confusion , lethargy, seizures, coma |
|
|
define: diuresis
|
- large volume of urine
- urine is dilute |
|
|
where is ADH synthesized?
|
- in the supraoptic and paraventricular nuclei of the hypothalamus
- packaged into granules - stored in the posterior pituitary |
|
|
which factors increase ADH secretion?
|
1. osmolality of body fluids (main)
2. volume and pressure of vascular system |
|
|
which cells sense changes in body osmolality?
|
- osmoreceptors
- found in the hypothalamus - only respond to solutes that are effective osmoles - when osmolality rises, the osmoreceptors signal the cells int eh supraoptica nd paraventricular nuclei to increase ADH secretion |
|
|
name an ineffective osmole
|
urea
|
|
|
how does ADH respond rapidly to body fluctuations in osmolality?
|
- it's broken down within minutes in the plasma
- sensitive control |
|
|
where are changes in blood pressure sensesd?
|
Baroreceptors:
1. high pressure: aortic arch and carotid sinus 2. low pressure: left atrium and pulmonary vessels - can stimulate ADH secretion - carried by the vagus and glossopharyngeal nerves to the solitary tract nucleus of the medulla oblongata |
|
|
what can cause SIADH?
|
1. infections and neoplasms of the brain
2. drugs (anti-tumor agents) 3. pulmonary diseases 4. carcinoma of the lung |
|
|
what are aquaporins?
|
- water channels (aquaporin 2) that are inserted into the apical membrane of the collecting duct principal cells in response to ADH
|
|
|
what causes nephrogenic diabetes insipidus?
|
- can be inherited
- most often caused by: - metabolic disorders (hypercalcemia) - drugs (lithium) |
|
|
what drug can cause nephrogenic diabetes inspidus?
|
lithium
|
|
|
how does ADH incrase permeability of the CD to urea?
|
- ADH phosphorylates the UT1 (apical membrane urea transporter) and lets it pass more urea inot the cell
|
|
|
where is the receptor for the V2 receptor?
|
- on the X chromosome
- X-linked |
|
|
where is the thirst center located?
|
- anterolateral region of the hypothalamus (not in the same as the osmoreceptors for ADH secretion)
|
|
|
where does the separation of solute and water excretion occur?
|
- in the TAL of Henle's loop
|
|
|
how do you make hypoosmotic urine?
|
- just make sure the nephron reabsorbs solute, and not let water follow
- reabsorption of solute occurs primarily in the TAL |
|
|
where is urea an effective osmole?
|
- in many portions of the nephron, where permeability is low
|
|
|
what do you see on ECG for hyperkalemia?
|
- initially, tall thin T waves
- prolonged PR interval, depressed ST, prolonged QRS |
|
|
what do you see on ECG for hypokalemia?
|
- prolonged QT interval
- inverted T wave - depressed ST |
|
|
which hormones increase K uptake into skeletal muscle, liver, bone and RBCs by stimulating the Na, K, ATPase pump?
|
- epinephrine, insulin, aldosterone
|
|
|
describe the adrenergic receptors and K regulation
|
- a-adrenergic receptor activation is necessary to prevent hypokalemia after exercise (release of K from cells)
- b2 receptors causes K uptake by cells |
|
|
which drug can cause increased levels of K after a meal?
|
- propranolol
- b adrenergic blocker - inhibits K uptake by cells |
|
|
what are the two routes by which aldosterone affects serum K levels?
|
1. stimulates urinary K excretion
2. increases K uptake into cells |
|
|
what pH disturbance causes a rise in plasma K?
|
- metabolic acidosis increases plasma K
- reduced pH stimulates movement of H into cells and K out of cells |
|
|
what pH disturbance causes a drop in plasma K?
|
- metablolic alkalosis decreases plasma K
|
|
|
what does hyperosmolality have on serum K levels?
|
- increases K release by cells -> increases extracellular K
(increased osmolality will cause water to leave cell, thereby concentrating the K within the cell, providing the driving force for K exit out of the cell) |
|
|
which diseases associated with cell lysis can cause an increase in serum K?
|
- burns
- tumor lysis syndrome - rhabdomyolysis |
|
|
how might exercise lead to life threatening hyperkalemia?
|
- if the person is also on b-adrenergic blockers, K is not taken up by cells
|
|
|
which drugs can cause hyperkalemia?
|
- potassium supplements
- ACE inhibitors - K sparing diuretics - heparin - prostaglandin-suppressing drugs (cuase hyporeninemic hypoaldosteronism) |
|
|
where is K excretion regulated?
|
- DISTAL TUBULE
- COLLECTING DUCT - able to both reabsorb or secrete K |
