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304 Cards in this Set

  • Front
  • Back
what are most glomerular diseases caused by?
- immunologically mediated
what are most tubular and interstitial diseases mediated by?
- toxic or infectious agents
when do you see prerenal azotemia?
- hypoperfusion of kidneys:
- hemorrhage
- shock
- volume deplition
when do you see postrenal azotemia?
- urine flow is obstructed below level of kidney
define uremia
- when azotemia becomes associated with clinical signs
what can there be secondary involvement of with uremia?
- GI system: uremic gastroenteritis
- peripheral nerves: peripheral neuropathy
- heart: uremic fibrinous pericarditis
what is acute renal failure?
- reduced or no urine flow (oliguria or anuria)
what clincal symptoms do you see in renal tubular defects?
- polyuria
- nocturia
- electrolyte disorders (met acidosis)
describe the four stages of chronic renal failure
1. diminished renal reserve
2. renal insufficiency
3. renal failure
4. end-stage renal disease
define: diminisehd renal reserve
- GFR is 50% normal
- BUN and creatinine are normla
- asymptomatic
- more susceptible to developing azotemia with additional renal insult
define: renal insufficiency
- 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
what may happen over time with a patient who's only got one kidney?
- progressive glomerular sclerosis in the remaining kidney as a result of adaptive changes in hypertophied nephrrons
why are ectopic kidneys predisposed to infection and obstruction to urinary flow?
- kinks in the ureters due to abnormal location
which genes are involved in polycystic kidney disease?
- chr 16: PKD1 -> polycystin-1
- chr 4: PKD2 -> polycystin-2
how do you explain both lung and kidney disease in Goodpasture syndrome?
- anti-GBM antibodies cross react with other BMs, esp in the lung alveoli
which antigens can cause circulating immune complex nephritis (not specific for the glomerulus)
- streptococci
- Hep B (HBsAg)
- Hep C
- treponema pallidum
- plasmodium falciparum`
what causes focal segmental glomerulosclerosis?
- adaptive change in the relatively unaffected glomeruli of diseased kidneys (think of agenic kidneys- same principle)
what is the prevalence of unilateral agenesis?
- relatively common (1 in 1000 births)
how does unilateral renal agenesis present?
- either completely asymptomatic
- or, seen with other congenital anomalies
- a single umbilical artery may clue you in to the diagnosis
what causes unilateral renal agenesis?
- failure of the uretic buds to develop
what happens with complete divison of a ureteric bud?
- bifid ureter with a double kidney on one side
what happens with crossed renal ectopia?
- fused kidneys on one side
what happens with double uretic buds?
- supernumerary kidney
what happens with incomplete division of a ureteric bud?
- bifid ureter with a partially divided kidney
what does the ureteric bud give rise to?
- ureter
- renal pelvis
- major and minor clayces
- 1-3 million collecting tubules
describe the Potter sequence
- 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
what can fibromuscular dysplasia (FMD) cause?
- can lead to bilateral renal artery stenosis (beaded appearance on angiography)
- mediated by an autoimmune response
- a type of vasculitis
define: angiography
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.
how do you treat renal stenosis caused by fibromuscular dysplasia?
- renal artery balloon angioplasty
what is the incidence of unilateral renal artery stenosis?
- relatively uncommon cause of hypertension
- responsible for 2-5% of cases of hypertension
how do you treat renal artery stensis?
- surgical treatment
- successful in 70-80% of patients
what happens with unilateral renal artery stenosis?
- hypertension that is equal in magnitude to the degree of stenosis
- initially, due to the increase in renin secretion
what is the most common cause of renal artery stenosis?
- in 70% of cases, is atheromatous plaque at the origin of the renal artery
what is the epidemiology of renal artery stenosis caused by artheromatous plaque?
- more frequent in men
- increases with age, and diabetes
what is the second most common cause of renal artery stenosis?
- fibromuscular dysplasia of the renal artery
- thickening of either the intima, media, or adventitia of the artery
what are the subclassifications of fibromuscular dysplasia?
1. intimal medial hyperplasia
2. adventitial hyperplasia
what is the epidemiology of fibromuscular dysplasia?
- more common in women
- tend to occur in younger age groups (30s-40s)
describe the progression of kidney ischemia
- 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
what causes double ureters?
- 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
what is a ureteropelvic junction obstruction?
- congenital disorder
- results in hydronephrosis
- usually presents in children
- more common in boys
why doesn't Angiotensin II decrease GFR since it causes peripheral vasoconstriction?
- Ang II also vasoconstricts the efferent arteriole -> maintains GFR even with reduced plasma flow
what happens to pH levels with renal artery stenosis?
- pH rises -> metabolic alkalosis due to increased net acid SECRETION from hyperaldosteronism
what happens to K with renal artery stenosis?
- K SECRETION increases due to increased levels of aldosterone
which part of the urinary system is involved if you see white cell casts in the urine?
- the kidneys
- leukocytes are compressed together in the renal tubules
where is the involvement if you see red blood cell casts?
- kidney
- compression of RBCs in the renal tubules
what are you concerned about when you see a UTI in a pregnant woman?
- spread to the uterus
what is a normal range for blood pH?
what are normal values for PCO2?
33-45 mmHg
what are normal values for PO2?
75-105 mmHg
what are normal fasting glucose levels in serum?
- 70-110 mg/dL
what are normal post-prandial serum glucose levels?
2 hours postprandial: <120mg/dL
what are normal plasma bicarb levels?
22-28 mEq/L
when do you get mixed acidosis?
- cardiopulmonary arrest
- have some lactic acidosis (metabolic)
- respiratory acidosis from ventilary standstill
what defines a metabolic acidosis?
- plasma pH and HCO3- are low
what defines a respiratory acidosis?
- plasma pH is low
- arterial CO2 is high
how do you calculate the volume of a fluid compartment?
- volume = (quantity of stuff administered)/(concentration of indicator in compartment)
where do you find p-ANCA?
sometimes seen in Goodpasture's syndrome patients
what causes Goodpasture Syndrome?
- autoantibodies against the noncollagenous domain of the a-3 chain of collagen 4
what is the epidemiology of Goodpasture Syndrome?
- occur in the teens and twenties
- more prevalent in MEN (in contrast to the other autoimmune diseases)
where do you see involvement for Goodpasture syndrome?
- inflammatory destruction of basement membrane in:
- kidney glomeruli
- lung alveoli
- gives rise to proliferative, rapidly progressing glomerulonephritis
- necrotizing hemorrhagic interstitial pneumonitis
what can trigger Goodpasture syndrome?
- environmental insult: virla infection, exposure to hydrocarbon solvens, smoking to unmask the cryptic epitose
what is the HLA association with Goodpasture Syndrome?
- HLA-DRB1*1501 and *1502
what do you see on histology in the lungs for Goodpasture syndrome?
- lungs are heavy with red-brown consolidation
- alveoli contain hemosiderin-laden macrophages
- lnear deposits of Ig along the BM of the septal walls
what do you see on histology in the kidneys for Goodpasture syndrome?
- focal proliferative glomerulonephritis
how does Goodpasture syndrome initially present? how do patients die?
- respiratory symptoms: hemoptysis
- focal pulmonary consolidations on X-ray
- most common cause of death: uremia
the ureter lies immediately anterior to which antatomical structure?
- the external iliac artery
where is the origin of the common iliac artery?
- bifurcation of the abdominal aorta
- occurs at the level of the 4th lumbar vertebra
where is the origin of the internal iliac artery?
- 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
where is the origin of the gonadal artery?
- abdominal aorta, usually between the renal artery and the inferior mesenteric artery
what tumor has dense immature islands of epithelial cells, spindled fibrolast-like stromal cells, and poorly formed tubular structures?
Wilms tumor
describe a Wilms' tumor
- neoplasm of the embryonic renal blastema
- has both neoplastic epithelial and stromal components
- have recognizable glomerular and/or tubular strucutres
describe a rhabdomyosarcoma
- cytoplasmic content of eosinophilic muscle proteins (thick and thin filaments)
describe a Ewing's sarcoma
- monotonous ball of primitive, small round cells with a thin rim of clear cytoplasm
- a tumor of bone
describe the clinical presentation of Hodgkin's disease
- lymphoid maligancy
- presents with lymphadenopathy of cervical and mediastinal nodes
- see inflammatory cells and Ree-Sternberg cells
how does a neuroblastoma present?
- frequently presents as an abdominal mass in children
are skeletal muscle neoplasms most often maligant of benign?
- malignant
- exception: cardiac rhabdomyoma
describe the epidemiology of rhabdomyosarcoma
- most common soft tissue sarcoma of childhood and adolescence
what are the classifications for rhabdomyosarcoma?
1. embryonal
2. alveolar
3. pleomorphic
describe the histology of rhabdomyosarcoma
- eccentric eosinophilic granular cytoplasm
- thick and thin filaments
- the cells can be round or elongated (tadpole or stap cells)
what is the most common type of rhabdomyosarcoma?
- embryonal (66%)
- variants: sarcoma botryoides, and spindle cell
describe embryonal rhabdomyosarcoma
- occurs in children under 10
- sheets of both malignant round and spindled cells in variably myxoid stroma
describe alveolar rhabdomyosarcoma
- common in mid-adolescence
- found in deep musculature of extremities
- on histology, the fibrous septae that divide cells into clusters looks like pulmonary alveoli
describe pleomorphic rhabdomyosarcoma
- rare
- found in deep soft tissue of adults
what is Ewing Sarcoma?
- 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
what is the epidemiology of Ewing Sarcoma and PNET?
- predilection for whites
- blacks are almost never affected
describe the morphology of Ewing Sarcoma and PNET
- 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)
how do Ewing Sarcoma and PNET present?
- painful enlarging masses
- tender, warm and swollen
what is a congenital disorder that results in hydronephrosis?
- ureteropelvic junction obstruction
describe ureteropelvic junction obstruction
- 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
what are the most common causes of UTI, in descending order?
1. E. coli
2. Proteus
3. Klebsiella
4. Enterobacter
what are the two ways in which bacteria can reach the kidneys?
- hematogenous infection: through the blood stream (less common in causing pyelonephritis)
- ascending infection: through the lower urinary tract
describe how hematogenous infection leading to pyelonephritis may occur
- seeding of kidneys from septicemia or infective endocarditis
how do you distinguish pre-renal failure from acute tubular necrosis?
- ADH is high in prerenal failure -> urea, water, and sodium resorption
what is the fractional sodium excretion in acute tubular necrosis and pre-renal failure?
- prerenal failure: Na excretion is <1%
- acute tubular necrosis: >2%
what is the normal ratio of BUN:creatinine?
- 12-20
- higher ratios are seen in prerenal azotemia
- lower ratios are seen in acute tubular necrosis
what are urinary sodium levels in prerenal failure?
- <20 mEq/L
what are urinary sodium levels in acute tubular necrosis?
- >40 mEq/L
what is urine osmolality in prerenal failure?
> 500mOsml/kg
what is urine osmolality in acute tubular necrosis?
< 350 mOsmol/kg
what is urine/serum creatinine in prerenal failure?
> 40
what is urine/serum creatinine in acute tubular necrosis?
what are the signs of bladder instability?
elderly woman presents with urinary urgency and incontinence
- 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
- choline-like compound that stimulates muscarinic receptors - can cause contraction of detrusor muscle
- indicated for treatment of urinary retention
- loop diuretic
- used to treat edema
- b1 selective antagonist
- used for hypertension and tachyarrhythmias
what two drugs do you not want to give with diabetes?
- metoprolol and glyburide
- metoprolol can mask hypoglycemia
- inhibits acetylcholine hydrolysis in synaptic cleft via ACh-esterase inhibition
- can cause detrusor muscle contraction
- used to treat urinary retention
- fluoroqunolone antibiotic for treatment of both gram-negative and gram positive bugs
- primarily used lower respiratory tract infections and UTIs
which drugs have been associated with arthropathy, myalgias, and leg cramps when given to children?
- lomefloxacin
- fluoroquinolone
azithromycin side effects
- macrolide antibiotic that is generally well tolerated
- mild nausea and abdominal pain
metronidazole side effects
- antiprotozoal and antibacterial
- convulsive seizures
- peripheral neuropathy
- can produce disulfiram like reactions when taken with alcohol
rifampin side effets
- used for TB and asymptomatic carriers of Neisseria meningitidis
- hepatotoxicity, hyperbilirubinemia, porphyria, cancer
tetracycline side effects
- antibiotic
- photosensitivity
- pseudotumor cerebri
- maculopapular rashes
what is derived from the ureteric bud?
- collecting system:
- collecting ducts
- minor and major calyces
- renal pelvis
what is derived from the metanephric mesoderm?
- ascending loop of Henle
- Bowman's capsule
- descendign loop of Henle
- glomerular tuft
what is a dangerous complication of a dissecting aortic aneurysm?
- bilateral renal infarction
- the dissecting aneurysm occludes both renal arteries -> bilateral renal infarction with flank pain and hematura
what can sickle cell crisis do to the kidneys?
- can cause papillary necrosis with hematuria
how do diuretics lead to aldosterone excess and hypokalemia? (method 1)
1. volume depletion stimulates aldosterone creation -> stimulates K excretion
how do diuretics lead to aldosterone excess and hypokalemia? (method 2)
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
how do diuretics lead to aldosterone excess and hypokalemia? (method 3)
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
what is the most common cause of metabolic alkalosis?
- thiazide or loop diuretics
which part of the renal vasculature is most vulnerable during a sickle cell crisis?
- vasa recta
- the high osmolarity of the renal medualla particularly favors sickling of erythrocytes
- can cause patchy papillary necrosis, proteinuria, and sometimes cortical scarring
what can sickling crises be triggered by?
- hypoxia from high altitude or pneumonia
why aren't glomerular capillaries involved during sickle cell crises?
- are small enough to be occluded, but are well oxygenated enough and the blood within them is not hypertonic
pseudomonas aeruginosa
- gram neg rol
- oxidase positive, lactose neg
- opportunistic - increase chance in causing UTIs in patients with indwelling catheters or who are on antibiotics
candida albicans
- yeast that can cause UTIs in poorly controlled diabetics b/c glucose in urine enhances growth
enterococcus faecalis
- gram + coccus
- causes UTIs in elderly men with prostate problems
E coli
- lactose positive
- oxidase negative
- gram neg rod
- common cause of UTIs
Klebsiella pneumoniae
- lactose positive
- oxidase neg
- gram neg rod
- causes UTIs in poorly controlled diabetics b/c glucose in urine enhances its growth
Proteus mirabilis
- gram neg rod
- member of the enterobacteriacaea family
- lactose neg
- contains urease -> splits urea to give ammonia -> raises pH of urine
which organisms are more likely to thrive if there are stones in the bladder?
- proteus mirabilis
- can hid in the stones and cause UTIs
- predisposes the development of stones
staphlococcus saprophyticus
- catalase positive
- coagulase neg
- gram positive coccus
- causes UTIs in young women
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
what is a common infection in patients with an indwelling bladder catheter?
- magnesium ammonium phosphate stones (with staghorn calculi) from urea-splitting bacteria
where are calcium-containing stones most frequently seen?
- in patients with hypercalcinuria WITHOUT hypercalcemia
- 1/5 of patients with calcium stones have hyperuricosuria
how do staghorn caliculi form?
- recurrent proteus infection
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)
what is the most common metabolic anomaly associated with urinary stones made of calcium phosphate or calcium oxalate?
- idiopathic hypercalcuria
what sort of stones can strict vegetarianism cause?
- increase oxaluria and formation of oxalate stones
what are normal sodium levels in the blood?
135-145 mEq/L
what are normal chloride levels in the blood?
95-105 mEq/L
what are normal potassium levels in the blood?
3.5-5.0 mEq/L
what are normal bicarbonate levels in the blood?
22-28 mEq/L
what are normal magnesium levels in the blood?
1.5-2.0 mEq/L
when is adequate replenishment of water loss by excretion interfered with?
- surgury
- can cause severe dehydration -> fever, psychic disturbances, death
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.
what is a 'finely granular' kidney surface indicative of?
- presence of arteriolonephroscloerosis (benign nephrosclerosis)
- caused by benign hypertension
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
what are the two forms of small vessel disease that are caused by hypertension?
1. hyaline arteriolosclerosis
2. hyperplastic arteriolosclerosis
describe hyaline arteriolosclerosis
- arteriolar wall is hyalinized
- lumen is narrowed
describe hyperplastic arteriolosclerosis
- onionskinning
- causes luminal obliteration
- secondary ischemic changes
- see wrinking of glomerular capillary vessels
who gets hyaline arteriolosclerosis?
- elderly patients, with or without hypertension
- more generalized and more sever in patients with hypertension
- also common in diabetes
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
when do you get hyperplastic arteriolosclerosis?
- seen in acute or severe elevations of blood pressure (e.g. malignant hypertension)
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
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
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
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)
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
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
what is IgA nephropathy also known as?
- Berger disease
what is Berger disease also known as?
- IgA nephropathy
what causes secondary IgA nephropathy?
- liver and intestinal diseases
- how do you diagnose IgA nephropathy?
- look for prominnet IgA deposits in the mesangial regions
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
- infections
- other autoimmune disorders
what drugs can cause membranous nephropathy?
- penicillamine
- captopril
- gold
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?
- 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
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?
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
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?

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?
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?
- able to both reabsorb or secrete K