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Renal pathophysiology Flashcards

1
Q

What are the stages of embryologic kidney development?

A

pronephros - week 4 (degenerates)
mesonephros - interim kidney during 1st trimester, contributes to male GU
metanephros - permanent kidney, first appears 5th week

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2
Q

What is the ureteric bud derived from and what does it give rise to?

A

derived from caudal end of mesonephric duct

gives rise to: ureter, pelvises, calyces, collecting duct; fully canalized by week 10

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3
Q

The metanephric mesenchyme and ureteric bud interacts to form what?

A

forms glomerulus through DCT

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4
Q

what can occur if there is poor interaction between metanephric mesenchyme and ureteric bud?

A

Multicystic dysplastic kidney

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5
Q

What is the most common site of obstruction in the fetus and why?

A

Ureteropelvic junction, last to canalize

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6
Q

What can cause Potter sequence (syndrome)?

A

Decreased ability of the fetus to produce urine:

ARPKD, obstructive uropathy (posterior urethral valves), bilateral renal agenesis

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7
Q

What is the pathogenesis and symptoms of of Potter sequence?

A

Renal failure in utero -> decreased amniotic fluid -> oligohydramnios –> fetus is compressed by muscular wall of uterus -> limb deformities

  • > facial anomalies (low-set ears and retrognathia)
  • > compression of chest and lack of amniotic fluid in lungs –> pulmonary hypoplasia (cause of death)
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8
Q

What causes horseshoe kidney?

A

inferior poles of both kidneys fuse together

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9
Q

Where do horseshoe kidneys lie in the abdomen?

A

Trapped under the inferior mesenteric artery therefore remain lower in abdomen than normal (near superior mesenteric artery)

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10
Q

What is horseshoe kidney associated with?

A

Kidneys function normally but associated with ureteropelvic junction obstruction, hydronephrosis, renal stones, infection

Chromosomal aneupolidy syndromes: Turner*, Edwards, Down, Patau

Rarely associated with renal cancer

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11
Q

What are the characteristics of multicystic dysplastic kidney

A

Caused by abnormal interaction btwn ureteric bud and metanephric mesenchyme

Leads to NONFUNCTIONAL kidney consisting of cysts and connective tissue

-if unilateral other kidney compensates and hypertrophies; bilateral = death

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12
Q

What is duplex collecting system?

A

Yshaped bifid ureter -> caused by either early bifurcation of ureteric bud before entering metanephric blastema or when 2 ureteric buds reach metanephric blastema

Associated with vesicoureteral reflux, ureteral obstruction, increase risk UTIs

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13
Q

At what level are the kidneys located?

A

T12-L3

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14
Q

Where does the kidney send sensory information to?

A

T10-T11 dermatomes –> CVA tenderness

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15
Q

Which kidney is usually taken during donor transplantation and why?

A

Left kidney bc it has a longer renal vein

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16
Q

What are the layers of the glomerular filtration barrier?

A

fenestrated capillary endothelium, basement membrane w/ heparan sulfate (neg charge barrier), podocytes

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17
Q

Where are the ureters in relation to the uterine artery and vas deferens?

A

ureters pass under uterine artery and under vas deferens

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18
Q

What are the % of body weight for total body water, intracellular fluid and extracellular fluid?

A

Total body water =60% body weight
ICF=40% body weight (2/3 of body water)
ECF=20% body weight (1/3 of body water)

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19
Q

what molecule can be used to measure plasma volume?

A

albumin

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20
Q

what molecule can be used to measure extracellular volume?

A

inulin

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21
Q

How is renal clearance calculated?

A

Cx=UxV/Px

Cx=clearance (ml/min)
Ux=urine concentration of X (mg/ml)
Px=plasma concentration of X (mg/ml)
V= urine flow rate (ml/min)

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22
Q

How is GFR calculated?

A

GFR=C inulin (approximated with creatine, but overestimates GFR)

GFR=Kf[(deltaP-deltaPoncotic)] delta=glomerular capillary - bowman space

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23
Q

How is effective renal plasma flow (eRPF) and renal blood flow (RBF) calculated?

A

eRPF=Upah x V/Ppah= Cpah pah=PAH (para-aminohippuric acid: filtered and secreted in PCT)

RBF=RPF/(1-Hct)

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24
Q

What is the filtration fraction (FF)?

A

FF=GFR/RPF = clearance of inulin (or creatine)/ clearance of PAH, normal FF =20%

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25
Q

How do NSAIDs affect the FF?

A

FF remains constant (prostaglandins preferentially dilate afferent arteriole so RPF and GFR both decrease with NSAIDs)

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26
Q

How do angiotensin II affect the FF?

A

FF increases since RPF decreases and GFR increases; AT II constricts efferent arteriole preferentially

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27
Q

Hartnup disease

A

AR, deficiency of neutral amino acid (like tryptophan) transporters in PCT cells and enterocytes -> decreased absorption from gut and increased secretion from kidneys -> low tryptophan for conversion to niacin –> pellagra

Treat with high protein diet and nicotinic acid

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28
Q

What is reabsorbed and secreted at the early PCT?

A

Reabsorbed: ALL glucose and amino acids, most HCO3-, Na+, Cl-, PO4-3, K+ and H2O

Secreted: NH3 and H+

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29
Q

What are the renal tubular defect syndromes?

A

FABulous Glittering LiquidS

FAnconi syndrome (PCT)
Bartter syndrome (thick ascending loop Henle)
Gitelman syndrome (DCT)
Liddle syndrome (collecting tubule)
Syndrome of apparent mineralocorticoid excess (collecting tubule)
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30
Q

Fanconi syndrome

A

Reabsorptive defect in PCT

Increased excretion of amino acids, glucose, bicarb and phosphate -> can cause metabolic acidosis (proximal renal tubular acidosis)

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31
Q

What can cause Fanconi syndrome?

A

hereditary defects (Wilson disease, tyrosinemia, GSD), ischemia, multiple myeloma, toxins/drugs (lead, expired teracyclines, tenofovir)

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32
Q

Bartter syndrome

A

AR reabsorptive defect in thick ascending loop of Henle, Defect of Na/K/2Cl co transporter

Causes hypokalemia and metabolic alkalosis with hypERcalciuria

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33
Q

What does Bartter syndrome mimic?

A

Loop diuretics

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34
Q

Gitelman syndrome

A

AR reabsorptive defect of NaCl in DCT

Less severe than Bartter syndrome; leads to hypokalemia, hypomagnesemia, metabolic alkalosis, hypOcalciuria

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35
Q

Liddle syndrome

A

AD, increased Na+ reabsorption in collecting tubules (Increased ENaC activity)

Causes HTN, hypokalemia, metabolic alkalosis, decreased aldosterone

Treatment: Amiloride (K+ sparring diuretic) Na+ channel blocker in collecting tubule

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36
Q

Syndrome of apparent mineralocorticoid excess

A

Increased Na+ reabsorption in collecting tubules

Deficiency of 11beta-hydroxysteroid dehydrogenase (converts cortisol to cortisone –> excess cortisol in cells -> increased mineralocorticoid receptor activity -> increased Na+ reabsorption -> HTN, hypokalemia, metabolic alkalosis, low aldosterone levels

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37
Q

How can syndrome of apparent mineralocorticoid excess be acquired?

A

glycyrrhetic acid (in licorice)

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38
Q

What does it mean if TF/P is >1, =1,

A

TF/P [tubular fluid]/[plasma]
TF/P>1 –> solute is reabsorbed less quickly than water (creatinine, Cl-, urea)
TF/P=1 –> solute is reabsorbed at the same rate as water (~Na+)
TF/P solute is reabsorbed more quickly than water (glucose, amino acids)

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39
Q

What stimulates renin release?

A 
low BP (JG cells)
low Na+ delivery (macula densa)
increased sympathetic tone (Beta1-receptors)
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40
Q

What affects does ACE have?

A

released by the lungs and kidney to convert angiotensin I to angiotensin II and also breaks down bradykinin

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41
Q

What are the 6 effects of angiotensin II?

A
  1. acts at angiotensin II receptor (AT1) on vascular smooth muscle -> vasoconstriction -> increase BP
  2. Constricts efferent arteriole -> increase FF and GFR
  3. stimulates release of Aldosterone from adrenals
  4. stimulates release of ADH from posterior pituitary
  5. increases PCT Na+/H+ activity to increase Na+, bicarb and water reabsorption
  6. Stimulates hypothalamus for thirst sensation
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42
Q

What are the effects of aldosterone on the kidney?

A

Regulates ECF volume and Na+ content; responds to low blood volume

increases Na+ channel and Na+/K+ pump insertion in principal cells and enhances K+ and H+ excretion —> Na+ and water reabsorption –> increased BP

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43
Q

What are the effects of ADH?

A

Regulates osmolarity

inserts aquaporin channels in principal cells -> increased water reabsorption -> increased BP

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44
Q

What are the effects of ANP and BNP

A

ANP released from atria and BNP released from ventricles in response to increased blood volume –> relaxes vascular smooth muscle via cGMP -> dilates afferent arteriole -> increases GFR and also decreases Renin

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45
Q

What releases EPO?

A

Interstitial cells (fibroblasts) in peritubular capillary bed

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46
Q

Where does the activation of vitamin D take place and what is the enzyme that does it?

A

PCT cells

25-OH D3 –> 1,25-(OH)2D3 via 1alpha-hydroxylase, stimulated by PTH

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47
Q

What are the effects of prostaglandins in the kidney?

A

paracrine secretion vasodilates the afferent arterioles to increase RBF

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48
Q

What are the effects of PTH?

A

increases Ca2+ reabsorption in the DCT

decreases phosphate reabsorption in the PCT

increases 1,25-(OH)2 vitamin D production in PCT by stimulating 1alpha-hydroxylase

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49
Q

What things cause K+ shift out of cells (hyperkalemia)?

A 
Digitalis (blocks Na+/K+ ATPase)
Hyperosmolarity
lysis of cells
acidosis
beta-blocker
hyperglycemia (insulin deficiency)
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50
Q

What things cause K+ shift into cells (hypokalemia)?

A

Hypo-osmolarity
alkalosis (K+/H+ exchanger increases K+ into cell and H+ out of cell)
beta-adrenergic agonist (increase Na+/K+ ATPase)
insulin (increase Na+/K+ ATPase)

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51
Q

What are symptoms of low serum Na+?

A

Nausea, malaise, stupor, coma, seizures

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52
Q

What are symptoms of low serum K+?

A

U waves on ECG, flattened T waves, arrhythmias, muscle spasm

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53
Q

What are symptoms of low serum Ca2+?

A

Tetany, seizures, QT prolongation

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54
Q

What are symptoms of low serum Mg2+?

A

Tetany, torsades de pointes, hypokalemia

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55
Q

What are symptoms of low serum phosphate?

A

bone loss, osteomalacia (adults), rickets (kids); phosphate needed for hydroxyapetite formation

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56
Q

What are symptoms of high serum Na+?

A

irritability, stupor, coma

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57
Q

What are symptoms of high serum K+?

A

wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness

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58
Q

What are symptoms of high serum Ca2+?

A 
stones (renal)
bones (pain)
groans (abdominal pain)
thrones (increase urinary frequency)
psychiatric overtones (anxiety, AMS)
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59
Q

What are symptoms of high serum Mg2+?

A

decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

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60
Q

What are symptoms of high serum phosphate?

A

renal stones, metastatic calcifications, hypocalcemia

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61
Q

Respiratory acidosis: what are the changes in pH, PCO2, bicarb and what are the causes?

A 
pH 40mmHg
bicarb high (compensatory)

Causes: hypoventilation (opioids, chronic lung disease etc)

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62
Q

Respiratory alkylosis: what are the changes in pH, PCO2, bicarb and what are the causes?

A

pH > 7.45

PCO2

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63
Q

Metabolic acidosis: what are the changes in pH, PCO2, bicarb?

A

pH

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64
Q

What is the equation for anion gap? What is considered normal?

A

Anion gap= Na+ – (Cl- + HCO3-) = 8-12 normally

65
Q

What are causes of increased anion gap metabolic acidosis?

A

MUDPILES

Methanol (formic acid)
Uremia
DKA
Propylene glycol
Iron/Isoniazid
Lactic acidosis
Etheylene glycol (oxalic acid)
Salicylates (late)
66
Q

What are causes of normal anion gap metabolic acidosis?

A

HARD-ASS

Hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea (both sodium and bicarb lost in stool)
Acetazolamide (carbonic anhydrase inhibitor)
Spironolactone (aldosterone antagonist)
Saline infusion

67
Q

What is the defect and urine pH in Distal (type 1) Renal Tubular Acidosis (RTA)

A

defect in secretion of H+ in alpha intercalated cells –> no bicarb generated –> acidosis

urine pH > 5.5

68
Q

What are the associations and causes of Distal (type 1) Renal Tubular Acidosis (RTA)

A

HypOkalemia -> increased risk for calcium phosphate stones (increased urine pH and bone turnover)

Causes: amphotericin B toxicity, analgesic nephropathy, obstruction of urinary tract

69
Q

What is the defect and urine pH in Proximal (type 2) Renal Tubular Acidosis (RTA)

A

defect in PCT bicarb reabsorption -> more bicarb excreted -> acidosis;

Urine becomes acidified in alpha-intercalated cells to compensate –> pH

70
Q

What are the associations and causes of Proximal (type 2) Renal Tubular Acidosis (RTA)

A

Associated with hypOkalemia, increased risk for hypophosphatemic rickets

Causes: Fanconi syndrome, carbonic anhydrase inhibitors, lead, aminoglycosides

71
Q

What is the defect and urine pH in Hyperkalemic (type 4) Renal Tubular Acidosis (RTA)

A

Defect: hypoaldosteronism -> hypERkalemia -> decreased NH3 synthesis in PCT -> decreased urea excretion

urine pH

72
Q

What are the associations and causes of Hyperkalemic (type 4) Renal Tubular Acidosis (RTA)

A

Hyperkalemia and hyperuricemia

Causes:
decreased aldosterone production (ACE inhibitors, ARBs, NSAIDs, diabetic hyoreninism, cyclosporine, adrenal insufficiency)

increased aldosterone resistance (K+ sparring diuretics, TMP/SMX, obstructive neuropathy)

73
Q

ADPKD

A
  • Autosomal dominant, mutation in PKD1 (chromosome 16) or PKD2 (minority of cases, chromosome 4)
  • Bilateral ENLARGED kidneys with numerous cysts in cortex and medulla
  • presents in young ADULTS as HTN, hematuria, renal failure
  • Associated with berry aneurysms, MVP, benign hepatic cysts
74
Q

ARPKD

A
  • Autosomal recessive, presents in INFANCY
  • Bilateral ENLARGED kidneys with numerous cysts in cortex and medulla
  • Significant renal failure in utero can cause Potter sequence
  • Associated with congenital hepatic fibrosis -> portal HTN and hepatic cysts
75
Q

Medullary cystic kidney disease

A

AD defect -> cysts in medullary collecting ducts

  • medullary cysts usually NOT visualized
  • tubulointerstitial fibrosis -> SHRUNKEN kidneys on US and progressive renal insufficiency
76
Q

What is the difference between simple and complex renal cysts?

A

Simple cysts: filled with UF (anechoic/dark on US). Common and usually asymptomatic

Complex cysts: septated, enhanced or solid components on US -> risk of RCC

77
Q

What are the types of acute renal failure?

A

prerenal azotemia, intrinsic renal failure (intrarenal azotemia), postrenal azotemia

78
Q

What causes prerenal azotemia?

A

Due to low renal blood flow - hypotension -> decreased GFR -> azotemia and oliguria

79
Q

What are the basic features of acute renal failure?

A

Severe decline in kidney function developing within days

Azotemia -> increased BUN and Cr and oliguria

80
Q

What are the clinical features of prerenal azotemia? - urine osmolarity, urine Na+, FENa, serum ratio BUN:Cr

A

urine osmolarity: >500 mOsm/kg (tubular fxn intact)

urine Na+: 15 (reabsorption of BUN due to increased aldosterone)

81
Q

What causes postrenal azotemia?

A

BILATERAL outflow obstructions -> stones, BPH, neoplasia, congenital anomalies

82
Q

What are the clinical features of early stage postrenal azotemia? - urine osmolarity, urine Na+, FENa, serum ratio BUN:Cr

A

EARLY stages:
urine osmolarity: >500 mOsm/kg (tubular fxn intact)
urine Na+: 15 (increased tubular pressure forces BUN into blood)

83
Q

What are the clinical features of late stage postrenal azotemia? - urine osmolarity, urine Na+, FENa, serum ratio BUN:Cr

A

LATE stages:
urine osmolarity: 40 (tubular fxn impaired)
FENa: >2% (tubular fxn impaired)
BUN:Cr decreased BUN reabsorbed)

84
Q

What causes intrinsic renal failure (intrarenal azotemia)?

A

Acute tubular necrosis, acute interstitial nephritis -> necrosis -> debris obstructs tubule -> decreased GFR –> urine has brown granular casts of dead epithelial cells

85
Q

What are the etiologies of acute tubular necrosis?

A

Ischemic -> decreased blood supply (HF, hypotension, sepsis, shock etc), preceded by prerenal azotemia

Nephrotoxic ->
drugs (aminoglycosides)
heavy metals (Pb)
myoglobinuria (muscle injury)
etheylene glycol (oxalate crystals in urine)
radiocontrast dye
urate (tumor lysis syndrome; avoid with hydration and allopurinol)

86
Q

What are the clinical features of acute tubular necrosis?

A

Oliguria with brown granular casts
Elevated BUN and Cr
Hyperkalemia with metabolic acidosis with increased anion gap

87
Q

What are the clinical features of intrinsic renal failure (intrarenal azotemia)? - urine osmolarity, urine Na+, FENa, serum ratio BUN:Cr

A

urine osmolarity: 40 (tubular fxn impaired)
FENa: >2% (tubular fxn impaired)
BUN:Cr decreased BUN reabsorbed

88
Q

What are the consequences of renal failure

A

MAD HUNGER

Metabolic Acidosis
Dyslipidemia (especially increased TAG)
Hyperkalemia
Uremia
Na+/H2O retention (HF, pulm edema, HTN)
Growth retardation
Erythropoietin failure (anemia)
Renal osteodystropy
89
Q

What is uremia?

A

Clinical syndrome of increased BUN:

  • nausea and anorexia
  • pericarditis
  • asterixis
  • encephalopathy
  • platelet dysfunction
90
Q

What are the mechanisms of renal osteodystrophy?

A

failure of vitamin D hydroxylation
-> decreased intestinal Ca2+ absorption

hypocalcemia (cant reabsorb calcium)

hyperphosphatemia (can’t excrete phosphate)

  • -> leads to secondary hyperparathyroidism
  • -> decreases serum Ca2+ by causing tissue calcifications
91
Q

What are the features of renal osteodystrophy?

A

Osteomalacia - cant mineralize osteoid due to low vitamin D

Osteoporosis (metabolic acidosis causes bone to be reabsorbed as buffer)

Ostetitis fibrosis cystica (secondary to hyperparathyroidism)- resorption of calcium destroys bone and fibrosis and cysts form

92
Q

What parts of the nephron are most susceptible to ischemic damage? nephrotoxic damage?

A

ischemic - PCT and loop of Henle

nephrotoxic - PCT

93
Q

What are the stages of ATN (acute tubular necrosis)?

A
  1. inciting event
  2. maintenance phase - oliguric; 1-3 weeks; risk of hypERkalemia, metabolic acidosis, uremia
  3. recovery phase - polyuric, BUN and Cr fall, risk of hypOkalemia
94
Q

Renal papillary necrosis - what does it cause and what is it associated with?

A

sloughing of necrotic renal papillae -> gross hematuria and proteinuria

Associated with:
Sickle cell disease/trait
Acute pyelonephritis
Analgesics (NSAIDs)
Diabetes mellitus
95
Q

What can cause diffuse cortical necrosis of the kidneys?

A

Usually combo of vasospasm and DIC

Associated with obstetric problems (abruptio placentae), septic shock

96
Q

What are the symptoms of acute bacterial cystitis?

A

suprapubic pain, dysuria, urinary frequency, urgency

*Systemic signs (fever, chills) usually ABSENT

97
Q

What are the lab findings of acute bacterial cystitis?

A 
Dipstick
\+ leukocyte esterase
\+ nitrites for gram(-) organisms
UA: cloudy urine w >10 WBCs/hpf
\+ culture (>100k colony forming units)
98
Q

What does a negative urine culture in suspected bacterial cystitis suggest?

A

Sterile pyuria and negative cultures suggest urethritis by N. gonorrhea or C. trachomatis

99
Q

What are the most common causes of acute bacterial cystitis?

A 
E. coli
Staph saprophyticus (sexually active young F)
Klebsiella
Proteus *urine has ammonia sent
Enterococcus faecalis
100
Q

What are the common causes of acute pyelonephritis?

A

Ascending infection of:
E. coli (90%)
E. faecalis
Klebsiella

101
Q

what are the clinical features of acute pyelonephritis?

A

Fevers, CVA tenderness
WBCs in urine +/- WBC casts

CT: striated parenchymal enhancement

102
Q

What are risk factors for pyelonephritis?

A

indwelling urinary catheter, urinary tract obstruction, vesicoureteral reflux, diabetes mellitus, pregnancy

103
Q

What are the features of chronic pyelonephritis?

A

*Thyroidization of kidney on H&E - tubules contain eosinophilic casts resembling thyroid tissue

asymmetric corticomedullary scarring, blunted calyx

104
Q

What are the causes and symptoms of drug-induced interstitial nephritis (tubulointerstitial nephritis)?

A

Pyuria and azotemia after drugs due to hypersensitivity
1-2 weeks after: diuretics, penicillin derivatives, PPIs, sulfonamides, rifampin
months after starting NSAIDs

Symptoms: fever, rash, hematuria, CVA tenderness; can also be asymptomatic

105
Q

What are the symptoms of kidney stones (nephrolithiasis)?

A

colicky pain with hematuria, CVA tenderness (unilateral)

106
Q

What are general risk factors for kidney stones?

A

low urine volume

high concentration of solute

107
Q

Calcium stones - what are the x-ray findings, precipitation pH and crystal shape?

A

X-ray: radiopaque
pH: alkaline pH for calcium phosphate crystals
acidic pH for calcium oxalate crystals
crystal: envelope or dumbbell shaped

108
Q

What causes calcium stones? What is the treatment?

A

usually idiopathic hypercalciuria (high calcium in urine but normal blood calcium levels)

Oxalate crystals can result from ethylene glycol ingestion, vitamin C abuse, hypocitraturia, malabsorption (Crohn disease)

Treatment: hydration, thiazides (ca2+ sparring diuretic), citrate (complexes with calcium)

109
Q

What causes ammonium magnesium phosphate (struvite) stones? What is the treatment?

A

commonly form struvite crystals

Caused by urease (+) bugs (proteus, staph saprophyticus, klebsiella) that hydrolyze urea to ammonia -> increases urine pH

Treatment: treat infection and surgically remove stone

110
Q

ammonium magnesium phosphate (struvite) stones - what are the x-ray findings, precipitation pH and crystal shape?

A

X-ray: radiopaque
pH: alkaline pH
crystal: coffin lid

111
Q

uric acid stones - what are the x-ray findings, precipitation pH and crystal shape?

A

X-ray: radiolucent** visible on CT and US but NOT X-ray**
pH: acidic pH
crystal: rhomboid or rosettes

112
Q

What causes uric acid stones? What is the treatment?

A

Risk factors: decreased urine volume, arid climates, ACIDIC pH

Most common stone in patients with gout, hyperuricemia (leukemia or myeloproliferative disorders)

Treatment: alkalinization of urine (potassium bicarb), allopurinol

113
Q

cystine stones - what are the x-ray findings, precipitation pH and crystal shape?

A

X-ray: radiopaque
pH: acidic pH
crystal: Hexogonal “SIXtine” stones have SIX sides

114
Q

What causes cystine stones? What is the treatment?

A

AR condition causing loss of fxn in cystine-reabsorbing PCT transporter –> cystinuria (cystine is poorly soluble)

mostly seen in children

Can form staghorn calculi

(+) Sodium cyanide nitroprusside test

Treatment: alkalinization (potassium bicarb) of urine and hydration

115
Q

Hydronephrosis - pathophysiology and findings

A

Causes: urinary tract obstruction (stones, BPH, cancer, injury), retroperiotneal fibrosis, vesicoureteral reflux

Presents with CVA tenderness and palpable mass in R/L upper quadrant

Dilation/distention of renal pelvis and calyces occur proximal to site of pathology -> imaged on US or CT

Cr only rises if bilateral or patient only has 1 kidney

116
Q

What are complications of hydronephrosis?

A

compression and possible atrophy of renal cortex and medulla

117
Q

What is nephritic-nephrotic syndrome and with what conditions is it most commonly seen?

A

nephritic syndrome with GBM damage that damages glomerular filtration charge barrier -> nephrotic proteinuria

Can occur with any nephritic syndrome, most commonly in: Diffuse proliferative GN and membranoproliferative GN

118
Q

What is nephritic syndrome? What are the common clinical features?

A

Glomerular inflammation and bleeding -> GBM disruption

Causes HTN, increased BUN and creatinine, oliguria, hematuria, RBC casts

proteinuria

119
Q

What is nephrotic syndrome? What are the common clinical features?

A

Podocyte disruption -> charge barrier impaired

Massive proteinuria >3.5g/day
Hypoalbuminemia -> edema
Hyperlipidemia and hypercholesterolemia
(some) Hypogammaglobulinemia -> increased infection risk
(some) Hypercoagulable state from loss of antithrombin III

120
Q

Acute poststreptococcal glomerulonephritis - What is the etiology and clinical features?

A

~2 wks post strep A infection of skin or pharynx; most frequently in children

Type III hypersensitivity reaction - M protein virulence factor causes immune complex deposition containing IgG, IgM and C3

Clinical features: Nephritic syndrome (urine protein

121
Q

Acute poststreptococcal glomerulonephritis - What are the LM, IF and EM features?

A

LM - glomeruli enlarged and hypercellular (inflammation)

IF - “starry sky” granular appearance “lumpy bumpy” due to IgG, IgM and C3 deposition along GBM and mesangium

*EM - subEPIthelial immune complex humps

122
Q

Rapid progressive glomerulonephritis (RPGN)- What is the etiology and LM features?

A

Nephritic syndrome that progresses to renal failure in weeks to months

H&E LM: crescents comprised of fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes and macrophages in Bowman space

Can be caused by several diseases:
Goodpasture syndrome
PSGN
diffuse proliferative glomerulonephritis
Wegener granulomatosis
microscopic polyangiitis
Churg-Strauss syndrome
123
Q

What is the etiology of RPGN with linear immunofluorescent staining?

A

IF pattern: linear -> Goodpasture syndrome (anti-basement membrane antibody) Type II hypersensitivity rxn

Antibody also against alveolar basement membrane –> presents as hematuria and hemoptysis in young adult male

124
Q

What are the etiologies of RPGN with granular immunofluorescent staining? How can they be differentiated?

A

granular IF: immune complex deposition

Etiology: PSGN (sub-EPIthelial deposition, MOST COMMON type of granular IF RPGN) or diffuse proliferative glomerulonephritis (sub-ENDOthelial deposition)

125
Q

What are the etiologies of RPGN with negative immunofluorescent staining? How can they be differentiated?

A

Wegener granulomatosis: PR3-ANCA/c-ANCA; affects lung, kidney and nasalpharynx

microscopic polyangiitis: MPO-ANCA/p-ANCA

Churg-Strauss syndrome: p-ANCA; differentiate from microscopic polyangiitis b/c also granulomatous inflammation, eosinophilia and asthma symptoms

126
Q

Diffuse proliferative glomerulonephritis (DPGN) - what is the etiology?

A

SLE or membranoproliferative glomerulonephritis –> nephritic syndrome

Most common type of renal disease in SLE and most common cause of death

DPGN and MPGN both present as nephrotic and nephritic syndromes concurrently

127
Q

Diffuse proliferative glomerulonephritis (DPGN)- What are the LM, IF and EM features?

A

LM: “wire looping” of capillaries

EM: subendothelial and sometimes intramembranous IgG-based immune complexes with C3 deposition

IF: granular

128
Q

What is the etiology and clinical features of IgA nephropathy (Berger disease)?

A

IgA immune complex deposition in mesangium -> nephritic syndrome

Presents in childhood as episodic gross or microscopic hematuria with RBC casts usually following mucosal infections (increased IgA produced)

Renal pathology of Henoch-Schonlein purpura

129
Q

IgA nephropathy (Berger disease)- What are the LM, IF and EM features?

A

LM: mesangial proliferation
EM; mesangial immune complex deposits
IM: IgA based immune complex deposits

130
Q

Alport syndrome - what is the etiology and clinical features?

A

X linked recessive mutation in type IV collagen -> thinning and splitting of GBM -> nephritic syndrome

Presents as hematuria, sensor hearing loss and ocular disturbances

“basket-weave” appearance on EM

131
Q

Membranoproliferative glomerulonephritis - Type I

A

Nephritic syndrome often copresenting with nephrotic syndrome

Associated with hep B and C

sub-endothelial immune complex deposits with granular IF

Thick basement membrane with ‘tram track’ appearance from GBM splitting by mesangial ingrowth

132
Q

Membranoproliferative glomerulonephritis - Type II

A

Nephritic syndrome often copresenting with nephrotic syndrome

Associated with C3 nephritic factor (stabilizes C3 convertase -> overactivation of complement and decreased serum C3 levels

intramembranous immune complex ‘dense’ deposits with granular IF

133
Q

Minimal change disease - etiology, epidemiology and treatment

A

Most common cause of nephrotic syndrome in CHILDREN
-usually idiopathic, associated with Hodgkin lymphoma (cytokine-mediated damage to podocytes -> disrupts filtration charge barrier)

Treatment: excellent response to steroids!

134
Q

Minimal change disease - LM, IF and EM characteristics

A

LM- NORMAL glomeruli, lipid may be seen in PCT cells

IF: negative

EM: effacement (fusion) of foot processes

135
Q

Focal segmental glomerulosclerosis - etiology, epidemiology and treatment

A

Most common cause of nephrotic syndrome in African Americans and Hispanics.

Idiopathic or secondary to other conditions: HIV, heroin use, sickle cell, interferon treatment, obesity, congenital CKD

Treatment: primary disease has inconsistent response to steroids

136
Q

Focal segmental glomerulosclerosis - LM, IF and EM characteristics

A

LM- Segmental (only part of glomerulus) sclerosis and hyalinosis

IF- nonspecific for focal deposits of IgM, C3, C1

EM- effacement of foot processes

137
Q

Membranous nephropathy- etiology, epidemiology and treatment

A

Most common cause of primary nephrotic syndrome in Caucasian adults

Idiopathic or secondary to other conditions:

  • antibodies to phospholipase A2 receptor
  • drugs: NSAIDs, penicillamine
  • infections: HBV, HCV
  • SLE (most common is diffuse proliferative GN)
  • solid tumors

Treatment: poor response to steroids

138
Q

Membranous nephropathy- LM, IF and EM characteristics

A

LM: diffuse capillary and GBM thickening

IF: granular due to immune complex deposits

EM: “spike and dome” appearance with subepithelial deposits

139
Q

Amyloidosis - nephrotic syndrome

A

Kidney is most commonly involved organ in systemic amyloidosis

Amyloid deposits in mesangium -> nephrotic syndrome

LM- congo red stain shows apple-red birefringence

Associated with chronic conditions like multiple myeloma, TB, RA

140
Q

Diabetic glomerulonephropathy

A

Nonenzymatic glycosylation of GBM -> lose charge barrier -> increase permeability, thickening

Nonenzymatic glycosylation of efferent arterioles -> increased GFR -> mesangial expansion

LM- mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)

141
Q

Renal angiomyolipoma is associated with what condition?

A

benign, hamartoma made up of blood vessels, smooth muscle and adipose tissue

*Increased frequencyin tuberous sclerosis

142
Q

Where does renal cell carcinoma arise from?

A

malignant epithelial tumor arising from kidney tubules

143
Q

How does renal cell carcinoma present clinically?

A

hematuria, palpable mass, CVA tenderness, secondary polycythemia (paraneoplastic syndrome increased EPO, renin, PTHrP or ACTH), fever, weight loss

144
Q

Who typically gets renal cell carcinoma?

A

Sporadic: adult men 50-70 years old, single tumor in upper pole of kidney; smoking and obesity

Hereditary: younger adults, bilateral tumors; increased risk with Von Hippel-Lindau disease (AD, inactivation of VHL -> risk of cerebellar hemangioblastoma and RCC)

145
Q

What is the pathogenesis of renal cell carcinoma? Where does it metastasize?

A

loss of VHL (3p) tumor suppressor gene -> increased IGF-1 (promotes growth) and increased HIF transcription factor (increases VEGF and PDGF -> angiogenesis)

Invades renal vein -> IVC -> metastasizes to lung and bone; can spread to retroperitoneal lymph nodes

146
Q

What are the gross and microscopic features of renal cell carcinoma?

A

Gross: yellow mass
Micro: polygonal clear cells

147
Q

What is the most common primary renal malignancy?

A

Renal cell carcinoma

148
Q

Renal oncocytoma

A

benign epithelial tumor

large eosinophilic cells with abundant mitochondria without perinuclear clearing (contrast to RCC)

presents with painless hematuria, flank pain and abdominal mass

149
Q

Wilms tumor (nephroblastoma) - what is it and who gets it?

A

malignant tumor comprised of blastema (immature kidney mesenchyme), primitive glomeruli and tubules, and stromal cells

Most common malignant renal tumor in children (avg age 3yo)

150
Q

Wilms tumor pathogenesis

A

loss of function mutations of tumor suppressor genes WT1 or WT2 on chromosome 11

151
Q

Beckwith-Wiedemann syndrome

A

Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy, organomegaly and macroglossia

Associated with mutations in WT2 (chromosome 11) gene cluster, especially IGF-2

152
Q

WAGR syndrome

A

Wilms tumor, Aniridia (absence of iris), Genitourinary malformation, mental Retardation

Associated with DELETION of WT1 tumor suppressor gene (11p13)

153
Q

Denys-Drash syndrome

A

Wilms tumor, progressive renal (glomerular) disease and male pseudohermaphroditism

associated with mutations of WT1

154
Q

Urothelial (transitional cell) carcinoma

A

Most common tumor of urinary tract system
Arises from urothelial lining and can occur in renal calyces, renal pelvis, ureters and bladder
–> usually the bladder

Major risk factors: smoking, azo/analine dyes, long-term cyclophosphamide or phenacetin use

Generally seen in older adults, presents with painless hematuria

155
Q

What are the 2 pathways of urothelial (transitional cell) carcinoma?

A
  1. flat, associated with early p53 mutations -> develops as high-grade flat tumor and then invades
  2. papillary (NOT associated with early p53 mutations) -> develops as low-grad papillary tumor-> progresses to high-grade -> invades
156
Q

Squamous cell carcinoma of the bladder - pathogenesis and risk factors

A

chronic irritation of bladder -> squamous metaplasia -> dysplasia -> squamous cell carcinoma

*presents as painless hematuria

Risk factors: chronic cystitis (older women), smoking, Schistosoma hematobium infection (Middle eastern men), chronic nephrolithiasis

157
Q

Adenocarcinoma of the bladder

A

arises from:

  • urachal remnant (tumor at dome of bladder, urachus connects fetal bladder to drain waste into yolk sac)
  • cystitis glandularis
  • exstrophy (congenital failure to form caudal portion of anterior abdominal and bladder walls)
158
Q

How is predicted respiratory compensation for a metabolic acidosis calculated?

A

Winter’s forumla:

PCO2 = 1.5[HCO3-] + 8 +/- 2

159
Q

Causes of increased K+ excretion

A
  1. High extracellular K+
  2. Increased aldosterone -> Na+ retained at expense of K+ loss
  3. Alkalosis (promotes K+ shift into cells for H+ exchange)
  4. Increased fluid flow through distal tubule-> quickly flushes away secreted K+

Renal (1 decks)

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