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Renal Flashcards

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1
Q

Sequence of Potter syndrome?

A 
Pulmonary hypoplasia
Oligohydraminios
Twisted face
Twisted skin 
Extremity defects 
Renal failure
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2
Q

What is oligohydraminos?

Causes?

A

Compression of developping fetus with limb deformities, facial anomalies (low set ears, retrognathia, flattened nose)

Compression of chest and lack of amniotic fluid aspiration into the fetal lungs

Can cause pulmonary hypoplasia

Causes:
ARPKD (polycystic kidney disease)
Obstructive uropathy
bilateral renal agenesis
Chronic placental insufficiency
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3
Q

Horeshoe kidney?

A

Inferior poles of the kidney are fused

Kidney’s function normally

Associated with hydronephrosis (uretropelvic obstruction, renal stones, infection, and chromosomal abnormality)

Associated with Turner’s syndrome, trisomies 13, 18, 21 and renal cancer

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4
Q

Unilateral renal agenesis?

A

Ureteric bud fails to develp and induce differentiation of metanephric mesenchyme

Complete absense of kidney and ureter

Often diagnosed with ultrasound prenatally

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5
Q

Multicyctic dyplastic kidney?

A

Ureteric bud fails to differentiare

Creates non functioning kidney consisting of cysts and connective tissue

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6
Q

What is duplex collecting system?

A

Bifurcation of ureteric bud before it enters the metanephric blastema

Y shaped bifid ureter

Strongly associated with vesicouretal refluc and ureteral obstruction

Increase risk of UTI

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7
Q

Congenital solitary functioning kidney?

A

Born with only one functioning kidney
Majority asymptomatic with compensatory hypertrophy of the contralateral kidney

Anomalies of the contralateral kidney are common

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8
Q

Which kidney taken during transplant?

A

Left kidney is taken, because it has a longer renal vein

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9
Q

Afferent vs efferent?

A

Afferent is arriving

Efferent is exiting

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10
Q

What is the renal blood flow?

A

Renal artery—segmental artery—interlobar artery—arcuate artery—interlober artery—afferent arterirole —-glomerus—-efferent arteriole—vasa rectal —peritubular capillaries—venous outflow

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11
Q

What is the course of the ureters?

A

Pass under uterine artery or under vas deferens (retroperitoneal)

Gynecological procedures (ligation of uterine or ovarian vessels) may damage ureter

Cause ureteral obstruction or leak

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12
Q

What are the percentage of the body composions?

A

(the percentage of body weight of a person)
60% total body water
40% ICF
20% ECF

Plasma volume can be measuredby radiolabeling albumin

Extracellular volume can be measured by insulin or mannitol

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13
Q

Glomerular filtration barrier?

A

responsible for filtration of plasma according size and net charge

Composed of fenestrated capillary endothelium

Fused basement membrane with heparin sulfate 
epithelial layer (negative charge and size barrier)

Epithlial layer consisting of podocyte foot processes (negative charge barrier)

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14
Q

What happens in the glomerular filtration barrier during nephrotic syndrome?

A

Albuinuriea
Hypoproteinemia
Generalized edema
Hyperlipidemia

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15
Q

How to calculate renal clearnace?

A

Cx (clearance of X)
Ux (urine concentration)
Px (plasma concentration)
V (urine flow rate)

If Cx < GFR (net resoprtion of X)
If Cx > GFR (net tubular secretion of X)
Cx = GFR no net secretion or absorption

How to calculate the volume ofplasma from which the substance is completely cleared per unit of time:

Cx= UxV/Px

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16
Q

What is a normal GFR?

How is GFR affected by stages of the kidney disease?

A

Normal GFR is 100 ml/minute
Incremental reduction of GFR that define stages of chronic kidney disease

Note: creatinine clearance is an approximate measure of GFR (slightly overestimates GFR because creatinine is moderately secreted by renal tubules

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17
Q

What is effective renal plasma flow?

A

Can be estimated using para-aminohippuric acid (PAH) clearence because between filtration and secretion, there is 100% secretion of all PAH that enters the kidney

eRPF = Upah x V/Ppah = Cpah

r

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18
Q

What is the renal blood flow?

A

RBF= RPF/ (1-Hct)

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19
Q

What is the plasma blood flow?

A

1-hematocrit

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20
Q

How does the eRPF compare to the renal plasma flow ?

A

The eRPF (effective renal plasma flow) underestimates the true renal plasma flow.

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21
Q

How to calculate filtration fraction?

A

FF= GFR/RPF (RPF is effective renal flow)

Normal FF is 20%

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22
Q

Effect GFR, RPF, and FF with afferent arteriole constriction?

A

GFR decreases
RPF decreases
No change in the FF (because FF is equal to GFR/RPF

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23
Q

Effect on GFR, RPF and FF if efferent arteriole constriction?

A

Increase GFR
Decrease RPF
Increase in FF

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24
Q

Effect of GFR, RPF abd FF increase plasma concentration?

A

Decrease GFR
No change in RPF
Decrease in FF

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25
Q

Effect on GFR, RPF and FF decrease in plasma?

A

Increase in GFR
No change RPF
increase FF

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26
Q

Effect on GFR, RPF, FF with constriction of ureter?

A

Decrease in GFR
No change in RPF
Decrease FF

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27
Q

Effect on GFR, RPF, FF with dehydration?

A

GFR decreases
RPf descreases
Increase FF

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28
Q

Normal range of glucose in the plasma levelÉ

A

Range is 60-120 mg per dl

Glucose should be completely resorbed in proximal convoluted tubule by Na+/glucose

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29
Q

At what glucose level does the transporters become saturated?

A

200 mg/dl

(this is when glucosuria begins) when all of the transporters are saturated

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30
Q

What happens to glucose during pregnancy?

A

Normal pregnancy decreases the ability of PCT to resorb glucose and amino acids

Leads to glucosuria and aminoaciduria

The proximal collecting tubule has a decreased ability to reasbosrb glucose

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31
Q

what does the proximal collecting tubule do?

A 
Resorbs:
Glucose
Amino acids
HCO3
Na
Cl 
PO3
K
H20
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32
Q

What does thin descending loop of Henle show?

A

Passively resorbs H2O via medullary hyetonicity (makes urine hypertonic)

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33
Q

what does thick ascending loop of Henle show?

A 
Reorbs:
Na
K 
Cl 
Mg
and Ca

Does NOTabsorb H2O

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34
Q

early Descending collecting tubule?

A

Resorbs
Na
Cl
Makes uring fully dilute (hypotonic)

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35
Q

what does the collecting tubule do?

A 
Resorbs:
Na
K 
H+
regulated by aldosterone
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36
Q

Fanconi defect?

A

Generalized defect in PCT
Increased excretion of amino acids (glucose, HCO3, Po43 and results in metabolic acidosis

Caused by hereditary defects (wilson disease, tyrosemia, glycogen storage disease, ischemia, multiple myeloma, nephrotoxins, lead poisoning

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37
Q

Barter syndrome?

A

Resorptive defect in thick ascending loop of Henle
Autosomal recessive
Affects Na/K/Cl
Results in hypokalemia, and metabolic acidosis with hypercalciuria

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38
Q

Gitelman syndrome?

A 
Resorptive defect NaCl in DCT 
Similar to lifelong thiazide diurectics 
Autosomal recessive 
Less severe then Barter syndrome 
Hypokalemia 
Hypomagneisum 
Metabolic alkalosis 
Hypocalciuria
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39
Q

Liddle syndrome?

A

Gain of function mutation
Increase Na resorption in collecting tubules
Presents like hyperaldosteronism
Aldosterone is nearly undetectable

Results in HTN
Hypokalemia 
metabolic alkalosis 
Decrease in aldosterone 
Treatment: amiloride
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40
Q

Syndrome of Apparent Mineralcorticoid excess?

A

Hereditary deficiency of 11B-hydroxysteroid dehydrogenase
(usually converts cortisol to cortisone)

Excess cortisol in the cells from enzyme deficiency

Increase mineralcorticoid receptor activity leading to HTN, hypokalemia, metabolic alkalosis

Treatment: corticosteroids —> decreases endogenous cortisol production and decrease mineralcorticoid activation

Cortisol tries to be the same as aldosterone

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41
Q

Relative concentrations along proximal convoluted tubules?

A

Tubular insulin increases in concentration along proximal collecting tubule due to water absorption

Cl reabsorption occurs at a slower rate then Na+ in early PCT and then matches Na+ resoprtion more distally

Relative concentration increases before it plateaus.

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42
Q

How does the Renin-Angiotensin-aldosterone system work?

A

renin secreted by the kidneys
Responsible for transforming angiotensinogen to angiotensin I

(ACE) produced by the lung and kidney to tranform angiotensin I to angiotensin II

Angiotensin II affects:
Vasoconstriction which increases the BP
Constricts efferent arteriole of glomerus (increases FF to preserve the renal function) in low volume states

Causes aldosterone secretion in the adrenal gland (increase Na2+ and Na/K) and creates a favorable gradient or Na+ and H20

Causes ADH secretion of the posterior pituitary:
Increases aquaporin (increases H2O resoprtion

Increases PCT absorption Na, HCO3 and H20 which can cause contraction alkalosis

Stimulates the hypothalamus leading to thirst

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43
Q

Fucntion of renin?

A

Secreted by JG cells in response to decrease renal arterial pressure and increase renal sympathetic discharge

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44
Q

Angiotensin II

A

Affects barorecptors function
Limits reflex bradycardia which would normally accompany the pressor effect

Helps maintain blood pressure and volume

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45
Q

ANP and BNP?

A

Released from atria ANP
And ventricles BNP in response to increase in volume
Relaxes smooth muscle cells via cGMP (icnrease GFR_ and decrease renin

Dilates afferent arteriole
Constricts efferent arteriole
Promotes natriuriesis

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46
Q

What does ADH do?

A

Regulates osmolarity

Responds to low blood volume states

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47
Q

What does aldosterone do?

A

Primarily regulares osmolarity (responds to low blood volume state)

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48
Q

Functions of juxtaglomerular appararus?

A

Jg secrete renin in response to decrease in renal blood pressure and increase in sympathetic tone

Macula densa cells sense decrease in NaCl delivery to DCT

Increase renin release
Cause efferent arteriole vasconstiction
Increase GFR

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49
Q

Mechanisms that cause shift of K out of the cell, and cause hyperkalemia?

A 
Digitalis (blocks the Na/K ATPase
HyperOsmolairty 
Lysis of cells (crush inhury, rhabdomyolysis, tumor lysis syndrome 
Acidosis 
B Blocker
High Blood sugar (insulin deficiency)
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50
Q

Process that shifts K into the cells causing hypokalemia?

A

Hypo-osmolarity
Alkalosis
B-Adrenergc (Na/K ATP ase)
Insulin (Increases Na/ K ATPase)

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51
Q

effects of low/ high Na?

A

Low:Nausea, Malaise, stupor, coma and seizures

High serum concentration: irritability, stupor, coma

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52
Q

High/low K?

A

Low: U waves are flattened T waves on ECG

High serum: wide QRS and peaked T waves on ECG, arrythmias, muscle weakness

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53
Q

High/Low Ca?

A

Low: tetany, Seizures, QT prolongation, Twitching (Chvostek sign)
Spasm(Trousseau’s sign)

High: Stones (renal)
Bones (pain)
Groans (abdominal pain)
Thrones: (increase in urinary frequency)
Pyschiatric overtones (anxiety, altered mental status)
Calciuria

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54
Q

High/low Mg 2?

A

Low: Tetany
Torsards
Hypokalemia

High:
Decrease in Deep tendon reflexes
Lethargy
Bradycardia
Hypotension 
Cardiac arrest
Hypocalcemia
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55
Q

High/low phosphate?

A

Low:
Bone loss
Osteomalacia (adults)
Rickets (children)

High:
Renal stones
Metastatic calcifications
Hypocalcemia

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56
Q

What are features of Barter syndrome?

A

No change in blood pressure
Increase plasma renin
Increase in aldosterone
Increase in urine Ca

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57
Q

What are the features of Gitelman syndrome?

A 
No change in blood pressure
Increase in plasma renin
Increase in aldosteron 
Decrease in serum Mg 
Decrease in urine Ca
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58
Q

Features of Liddle Syndrome?

A

Increase blood pressure
Decrease in renin
Decrease in aldosterone

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59
Q

Features of SIADH?

A

Increase in blood pressure
Decrease in plasma renin
Decrease in aldosterone

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60
Q

Primary hyperaldosterone (Conn syndrome)

A

Increase in blood pressure
Decrease in plamsa renin
Increase in aldosterone

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61
Q

Features of Renin-secreting tumor?

A

Increase in blood pressure
Increase in plasma renin
Increase in aldosterone

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62
Q

What is metabolic acidosis?

A

Decrease in pH
Low Co2
Low HCO3

Compensation with hyperventilation

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63
Q

Metabolic alkalosis?

A

Increase in pH
Increase in PCO2
Increase in HCO3
Compensation with hypoventilation

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64
Q

Respiratory acidosis?

A

Decrease in pH
Increase in PCO2
Increase in HCO3

Increase renal absoprtion of HCO3 (resorption is delayed)

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65
Q

Respiratory alkalosis?

A

Increase in pH
Decrease in PCO2
Decrease in HCO3

Compensatory: Decrease in renal HCO3 (resorption is delayed)

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66
Q

What are the steps of interpreting acid/base equations?

A

1) Look at the pH (less then 7.35 is acidic) and more the pH 7.45 is basic
2) Look at the PCO2 (is it more of left then 35)
3) Look at if the HCO3 is going in the same direction

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67
Q

What are functions of erythropoeitin?

A

Released by intersitial cells on the peritubular capillary bed in response to hypoxia

Stimbulates RBC production in the bone marrow

Can be supplemented in chronic kidney disease

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68
Q

Function of caciferol?

A

Proximal collecting cells convert 25-OH vitamin D3 to 1.25-(OH)2 vitamin D3 (calcitriol, active form)

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69
Q

Functions of prostaglandins?

A

Paracrine secretion vasodilates the afferent arteriorles to increase renal blood flow

NSAIDs will block renal protective prostaglandin synthesis leading to constriction of afferent arterirole and decrease GFR

This may result in acute renal failure in low renal blood flow states

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70
Q

Functions of dopamine?

A

Secreted by proximal collecting tubule cells
Promotes naturesis
At low doses dilates interlobular arteries, afferent arterioles and efferent arterioles
Increase in renal blood flow
Little or no change in GFF

At higher doses acts as vasoconstriction

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71
Q

Function of parathyroid hormone on the kidney?

A

Secreted in response to
Decrease in plasma Ca
Increase in plasma PO4
Decrease in 1.25 OH2D3

Causes: 
Increase in CA absorption (DCT) 
Decrease in PO4 resorprtion PCT
Increase in 1.25 D3 production 
Increase in Calcium and PO4 absortion from the gut (v ia vitamin D)
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72
Q

What does aldosterone do?

A

Secreted in response to decrease in blood volume via AT II

Increase in plasma K
Causes increase in Na reabsorption
Increase in K secretion
Increase in H+ secretion

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73
Q

what causes potassium out of the cell (causing hyperkalemia)?

A 
Digitalis (blocks Na/ K/ ATP ase
Hyperosmolarity
Lysis of cells (crush injury, rhabdomyolysis) 
Acidosis
B blocker
High blood sugar (insulin deficiency)
74
Q

What causes K to shift inside the cell (causes hypokalemia)?

A 
Hypo-osmolarity 
Alkalosis 
B adrenergic agonist (increase in NA/K+ ATPase)
Insulin (increase in Na+/K ATPase) 
Insulin shifts K+ into the cells
75
Q

Low Na concentration?

A 
Nausea
Malaise
Stupor
Como 
Seizures
76
Q

High Na concentration?

A

Irritability
Stupor
Coma

77
Q

Low Ca concentration?

A 
Tetanty
Seizures
QT prolongation
Twitching 
Chovostek sign
Spasm
Trousseau's sign
78
Q

High Ca concentration?

A 
Stones (renal)
Bones (pain) 
Groans (abdominal pain)
Thrones (increase urinary frequency)
Psychiatric overtones (anxiety, altered mental status)
Not necessarily calciuria
79
Q

Low magnesium concentration?

A

Tetany
Torsades de point
Hypokalemia

80
Q

High Mg Concentration?

A 
Decrease in deep tendon reflexes
Lethargy 
Bradycardia 
Hypotension
Cardiac Arrest
Hypocalcemia
81
Q

Low phosphate concentration?

A

Bone loss
Osteomalacia (adults)
rickets (children)

82
Q

High phosphate concentration?

A

Renal stones
Metastatic concentrations
Hypocalcemia

83
Q

Features of Barter Syndrome?

A

BP unchanged
Increase plasma Renin
Increase in aldosterone
Increase in urine Ca

84
Q

Features of Gitelman syndrome?

A 
No change in blood pressure
Increase in plasma renin 
Increase in aldosterone 
Decrease in serum MG
Decrease in calcium
85
Q

Features of Liddle syndrome?

A

Increase blood pressure
Decrease plasma rernin
Decrease aldosterone

86
Q

Features of SIADH?

A

Increase BP
Decrease plasma renin
Decrease aldosterone

87
Q

Features of primary hyperaldosterone (Conn)

A

Increase in BP
Decrease in renin
Increase aldosterone

88
Q

Features of renin secreting tumor?

A

Increase BP
Increase Renin
Increase Aldosterone

89
Q

Reaction to metabolic acidosis?

A

Hyperventilation (immediate)

90
Q

Reaction to metabolic alkalosis?

A

Hypoventilation (immeditae)

91
Q

Reaction to respiratory acidosis?

A

Increase in ranal HCO3 resoprtion

92
Q

Reaction to respiratory alkalosis?

A

Decrease in renal absorption of HCO3 (delayed)

93
Q

What is the formula to measure the respiratory compensation?

A

PCo2 = 1.5 (HCO3) + 8

IF measured CO2 is higher then predicted PCO2 (concomittant respiratory acidosis)

If measured CO2 is less then predicted PCO2 then comcomittant respiratory alkalosis

94
Q

Causes of respiratory acidosis?

A 
Airway obstruction
Acute lung disease 
Chronic lung disease Opiods
Sedatives
Weakening of respiratory muscles
95
Q

Causes of metabolic acidosis?

A

Depends on the anion gap ( Na- (Cl + HCO3)

>12 meq
MUD PILES
Methanol 
Uremia 
Diabetic ketoacidosis
Propylene glycol
Iron tablets or INH
Lactic acidosis
Ethylene glycol
Salicylates 
Anion gap from 8-12
HARDASS
Hyperalimentation
Addision disease
Renal tubular acidosis
Diarrhea
Acetazlaminde
Spironolactone
Saline Infusion
96
Q

Causes of respiratory alkalosis?

A 
Hyperventilation 
Hysteria
Hypoxemia 
Salicylates
Tumor 
Pulmonary embolism
97
Q

Causes of metabolic alkalosis?

A

Loop diuretics
Vomiting
Antacid use
Hyperaldosterone

98
Q

Characteristics of distal renal tubular acidosis?

A

Urine pH is more then 5.5
Defect in ability of the alpha intercalated cells to secrete H+
No new HCO3 is generated so leads to metabolic acidosis
Associated with hypokalemia
Increase risk for calcium phosphate kidney stones

Causes:
Amphotercin B toxcitiy
Analgesic nephorpathy
Congenital abnoramlities of the urinary tract

99
Q

Proximal renal tubular acidosis (type 2)?

A

Urine pH less then 5.5
defect in HCO3 absoption
Increased excretion of the HCO3
Associated with hypokalemia

100
Q

Hyperkalemia renal tubular acidosis?

A 
Urine Ph <5.5
Hypoaldosteronism
Hyperkalemia 
Decrease synthesis of NH3 in PCT 
Decrease in NH4 secretion 
Causes:
Decrease aldosterone production (diabetic hyporeninism)
ACE inhibitors
ARBS
NSAIDS 
Heparine
Cyclosporine
Adrenal insufficiency
Aldosterone resistence
TMP/SMX
101
Q

what do casts in the urine symbolize?

A

That hematuria.pyuria is of glomerular or renal tubular in origin

Bladder cancer, and kidney stones have hematuria with no casts

Acute cystis (pyuria, no casts)

102
Q

what do RBC casys suggest?

A

Glomerulonephrotos

Malignant hypertension

103
Q

what do WBC casts show?

A

Tubulointerstitial inflammation
Acute pyelonephritis
transplant rejectuon

104
Q

what do fatty casts show?

A

Nephrotic syndrome (associated with Maltese Cross sign)

105
Q

what does granular (muddy casts)

A

Acute tubular necrosis

106
Q

what do waxy casts whow?

A

End stage renal disease /chronic renal failure

107
Q

what do hyaline cases show?

A

Non specific
Normal finding
Seen in concentrated urine samples

108
Q

Focal glomerular disease?

A

Less then 50% of glomeruli are involved

Focal segmental glomeruloscloerosis

109
Q

Diffuse?

A

more then 50% of glomeruli involved

Diffuse proliferativ glomerulonephrites

110
Q

Proliferative?

A

Hypercellular glomeruli

Membranoproliferative glomerlonephrities

111
Q

Membraneous?

A

Thikcening of glomerular basement membrane (exapmle membraneous nephropathy)

112
Q

Primary glomerular disease?

A

Primary disease of the kidney that affects the glomeruli

example: minimal change disease

113
Q

What is Nephritic syndrome?

A 
Due to GBM disruption 
Symptoms include:
HTN
Increase in BUN and creatinine
Oliguria
Hematuria 
RBC casts in urine
Protinuria in subnephrotic range < 3.5 d/day 
But in severe cases may be in nephortic range
114
Q

What are the types of Nephritic syndrome?

A 
Acute poststeptoccocal glomerulonephritis
Rapidly progressive glomerulonephritis
IgA nephropathy (Berger disease)
Alport syndrome 
Membranoproliferative glomerulonephritis
115
Q

What are characteristics of nephrotic syndrome?

A 
Podocyte disruption
Change barrier impaired
Massive protinuria ( > 3.5 g/day)
with hypoalbunemia
hyperlipidemia 
Edema 
May be primary due to podocyte damage 
Secondary due to podocyte damage from systemic process like diabetes
116
Q

What are the types of nephortic syndrome?

A 
Focal segmental glomerulosclerosis (1 or 2)
Minimal change disease (1 or 2) 
Membraneous nephropathy (1 or 2)
Amyloidois (2) 
Diabetic glomerulonephopathy
117
Q

What are characteristics of nephritic-nephrotic syndrome?

A

Severe nephritic syndrome with GBM damage
This can result in damage of the glomerular filtration charge barrier

Nephrotic-range protinuria > 3.5 g/day

Comcomittant features of nephrotic syndrome
Can occur with any form of nephirtic syndrome

118
Q

what is the difference between the nephrotic and nephritic syndrome?

A

Primarily it is the amount of protein secreted
Nephritic is 0.25 range
The nephritic-nephortic is in the middle at around 35 g/ day
And the nephotic is high at over 35 grams per day

119
Q

Nephritic syndrome characteristics?

A

It is an inflammatory process
Involve glomeruli
Leads to hematuria and RBC casts in the urine
Assocaited with azotemia, oliguria, HTN (due to salt retention) and protinuria

120
Q

Characteristics of acute poststreptoccal glomerulonephritis?

A

Glomeruli will be enlarged and hypercellular
Granular appearence due to IgG and IgM, C3 deposition along GBM and mesangium
Has subepithelial immune complex in humps

Most frequently seen in children
Occurs 2-4 weeks after group A infection of the pharynx or skin

Resolves spontaneously (type 3 hypersensitivity reaction)

Presents with periphereal and periorbital edema
Can have cola colored urine
HTN

Will have positive strep titers/serologies
Decrease complement levels due to consumption

121
Q

Characteristics of Rapidly Progressive (Concentric) glomerulonephritis ?

A

Cresecent moon shape
Consist of fibrin and plasma proteins

Several disease processes may resuly in pattern

Poor prognosis because has rapidly deteriorating function (days to weeks)

For example: GOOD PASTURE SYNDROME

122
Q

What is good pasture syndrome characteristics?

A

Type II hypersensitivity
Antibodies to the GM membrane and alveolar basement membrabe

Granulomatosis with polyangiitis
Microscoptic polyangiitis

Need to do hematuria/hemoptysis
Treatment with emergent plasmapheresis

PR3-ANCA/ c-ANCA Pauci immune ( no Ig/C3) deposition

MPO-ANCA/p-ANCA (no Ig/C3 deposition)

123
Q

What are characteristics of diffuse proliferative glomerulnephritis ?

A

Show wire-looping of capillaries
Subendothelial and IgG-based IC with C3 deposition

This is a common cause of death in SLE (think wire lupus)

124
Q

Characteristics of IgA nephopathy>

A

Mesangial proliferation
Mesangial IC deposits
IgA based IC deposits in mesangium
Renal pathology of Henoch-Schonlein purpura

Episodic gross hematuria that occurs with respiratory or GI tract infections

Not to be confused with Beurger’s disease

125
Q

What are characteristics if nephritic syndrome?

A

Alport syndrome: mutation in IV collagen
Thinning and splitting glomerular basement membrane
Most commonly X-linked dominent

Will have eye problems (retinopathy and lens discoloration leading to sensineural deafness)

Membrano-proliferative glomerulonephritis?
Type 1-subendothelial immune complex with granular IF appearence on PAS strain

H& E stain (due to GBM splitting) caused by mesangial in growth

Type II: called dense deposit disease

This type of syndrome is usually seconday to hepatitis B or C infection (may also be idopathic)

Type III:associated with C3 nephritic factor (stabilizes C3 convertase and decrease C3 levels)

126
Q

what is minimal change disease?

A

Normal glomeruli
Effacement of foot processes
Commonly seen in nephrotic syndrome in children
Usually idiopathic (triggered by infection, immunization, immune stimulus)

Rarely can be secondary to lymphoma

Disease responds well to corticosteroids

127
Q

What are characteristics of focal segmental glomerulossclerosis ?

A

Segmental sclerosis and hyalinosis
Often - but have non specific focal deposits of IgM, C3, C1
Effacement of foot processes similar to minimal change disease

Most common cause of nephrotic syndrome in African American and Hispanics

Can be idiopathic
Secondary to other conditions:
HIV infection
Sickle cell disease 
Heroin abuse 
Obesity 
Interferon treatment 
Chronic kidney disease due to congential malformations

Primary disease has inconsistant response to steroids

128
Q

Membranous nephropathy

A

Diffuse capillary and GBM thickening
Can be granular as a result of immune complex deposition
Nephortic syndrome presentation of SLE
Has a spike and dome appearence with epithelial deposits

Most commo cause of nephortic syndrome in Caucausion adules

Can be due antibodies or to phospholipase A receptor
Can be secondary to drugs (NSAIDS and penicliin)
Infecions
SLE
Solid tumors
Primary disease has poor response to steroids
May progress to chronic conditions that predispose to amyloid deposits

129
Q

Characterstics of Amyloidosis?

A

Congo stain will show apple green birfirengence
Kidney is the most common involved organism
Associated with chronic conditions that predispose to amyloid deposition

130
Q

Characterstics of Diabetic glomerulonephropathy?

A

Non enzymatic glycosylation of GBM (increase in permeability and thickening)
Non enzymatic glycosylation of efferent arterioles (increase GFR leading to mesangil expansion)

This is most common cause of end stage renal disease in the US

131
Q

Kidney stone?

A

Severe complications such as hydronephoris, pyelonephritis
Presents with unilateral flank tendencies
Colickly pain that radiates to the groi

Kidney stones are usually made of calcium oxalate stones in patient with hypercalucuria and normocalcemia

132
Q

Type of stone: Calcium?

A

Calcium oxalate (hypocitratuira)
Usually radio-opaque
CT radioopaque
Shaped like a envelope or a dumbelle

Calcium stones are most common at 80%
Calcium oxalate more common then calcium phosphate.

Can result from ethylene glycol (anti-freeze) ingestion
Vitamin C
Hypocitraturia
Malabsorption

Treatment: Thiazides
Citrate
Low sodium diet

Calcium phospate:
Increasae in pH
Radio-opaque
Wedge shaped

133
Q

Ammonium magnsium phospahte stone?

A 
Increase the pH 
Radiopaque
Usually the shape of a coffin lid
Accounts for 15% of stones 
Caused by infection with urase +  bugs like proteus mrabilis (because they hydrolyze urea to ammonia)

Treatment: eradication of underlying infection
Surgical removal of stone

134
Q

Uric acid kidney stones?

A

Decrease in pH
Radiolucent
Minimally visible
Rhomboid or rosettes

About 5% of all stones 
Risk factors:
Decrease in urine 
Volume 
Arid climates
Acidid pH
Visible on ultrasound 
Often seen in diseases that increase cell turnover  (leukemia)

Treatment: Alkalization of urine
alopurinol

135
Q

Cysteine stones?

A

Decrease in pH
Radiolucent stone
Sometimes visible
Hexagonal

Hereditary autosomal recessive 
Cystien reasbsorbing PCT transporter
Loses function 
Causes cystinuria 
Transportor defect also results in poor absorption of Ornithine, lysine, arginne (COLA) 
Cystine is poorly soluable 
Stones form in urine 
Usually begins in childhood 
Form staghorn calculi
Sdoim cyanide

SIXtine stone hbe six sides

Treatment: low sodium diet
alkanization of urine
Chelating agents if refractory

136
Q

What is hydronephorsis?

A

Distention of renal pelvis and calycees
Usually caused by urinary tract obstruction (renal stones, BPH, cervical cancer, injury to ureter)

Can also be caused by retroperitoneal fibrosis
Vesicureteral reflux
Dilatation occurs proximal to the site of pathology
Serum creatinine becomes elevated only if obstruction is bilateral or if patient only has one kidney

Leads to compression
Atrophy of the renal cortex and medulla

137
Q

Renal cell carcinoma?

A

Originates from the PCT (polygonal clear cells)
Polygonal clear cells
Usually golden yellow (due to increase lipid and carbohydrate)
Usually in men 50-70 years old
Increase incidence with smoking and obesity

Clinically: hematuria and palpable mass

Invades the renal vien and then the IVC, spreads hemtogenously

Mets to the lung and the bone

Treatment:
Ressection if localized disease

Immunotherapy (aldesleukin) or targeted therapy for advanced, metastatic disease

Resistent to chemotherapy and radiation therpy

Most common is primary renal malignancy

Associated with gene deletion on chromosome 3 or inheritied as von Hippel-Lindau syndrome

Associated with paraneoplasyic syndromes (ectopic EPO, ACTH, PTHrP, renin)

Silent cancer that often presents as metastatic neoplasm

138
Q

Renal Oncocytoma?

A

Benign cell tumor arising from the collecting ducts
Usually well circumscribed mass with central scar
Large eosinophilic cells with abundunt mitochrondria without perinuclear clearing

Presents with painless hematuria (flank pain) and abdominal mass

Often ressected to exclude malignancy (renal cell carcinoma)

139
Q

Characteristics of Wilms Tumor?

A

Most common malignancy of early childhood (ages 204)
Contains embryonic glomerular structues
Large, palpable unilateral flank mass

Genetic basis: loss of suppressor genes (WT1 or WT2) on chromosome 11

140
Q

What is the WAGR complex?
Deny-Drash syndrome?
Beckwith-Wiedemann?

A

Wilms tumor
Aniridia (absence of iris)
Genitourinary malformation
Mental retardation

Denys-Drash: wilms tumor, early onset nephrotic syndrome
Male pseudohermaphroditism

Beckwith-wiedmann: Wilms tumor,macroglossia, organomegaly, hemihypertrophy

141
Q

What are characteristics of transitional cell carcinoma?

A

Common tumor of the urinary tract (occurs in renal calyces, renal pelvis, ureters, and bladder)

Painless hematuria without casts (suggest bladder Ca)

Associated with Phenacetin, smoking, aniline dyes, cyclophaspchamide

142
Q

Characteristics of squamous cell carcinoma of the bladder?

A

Due to chronic irritation of the bladder
Leads to metaplasia to dysplasia to squamous cell carcinoma

Risk factors include: Schistoma haematobium infection (middle east) chronic cystitis, smoking, chronephorlithiasis

Risk factors include: Schistoma haematobium
Chronic cystitis, smoking, chronic nepholithiasis

Presents with painless hematuria

143
Q

List the 4 types of urinary incontinence?

A

Stress incontinence
Urgency incontinence
Mixed incontinene
Overflow incontinence

144
Q

Characteristics of stress incontinence?

A

Outlet incompetnece (uretheral hypermobility or intrinsic shincteric defiecency)

Leak with increase in intra-abdominal pressure (sneezing and lifting)

Increase risk with obesity
vaginal delivery
Prostate surgery
Have a positive bladder test (will obsreved leaking upon coughing or valsalva)

Kegal and pelvic floor strengtheing

145
Q

Characteristics of urgency incontinence?

A 
Overactive bladder (detrusor instability) 
Leak with the urge to void immediately
Treatment is Kegal exercises 
Bladder training (timed voiding and distraction or relaxtion techniques)

Can treat with

146
Q

Mixed incontinence?

A

Features of both stress and urgency incontinence

147
Q

Characteristics of overflow incontinence?

A

Incomplete emptying (detrusor underactivity or outlet obstruction)

Leak with overfilling
Increase in post void residual
Will have urinary retention on catherization or ultradsound

Treatment with catherization or relieve obstruction ( alpha-blocker for BPH)

148
Q

Characteristics of urinary tract infection?

A

Presents with dysuria, urinary frequency and urgency
Usually o systemic signs

Risk factors:
Female gender
Sexual itercourse (honeymoon cystitis)
Diabetes mellitus
Impaired bladder emptying 
Causes:
E Cholic
Staph saprophyticus
Klebsiella
Proteus Mirabilis  (has an ammonia scent)

Lab findings:
+ leukocyte
+Nitrates (usually gram negative organisms E choli)
Sterile pyuria
negative urine culture suggests urethritis
(Neisseria gonorrhea or chlamydia trachomatis)

149
Q

What are signs of acute pyelonephritis?

A

Neutrophils that infiltate the renal interstium
Affects the cortex and spares the glomeruli/vessels
Presents with fever, flank pain
Costavertebral tenderness
Nausea and vomiting
Causes vesicoureteral reflux

Complications:
Chronic pyelonephritis 
Renal papillary necrosis 
Perinephric abcess
Urosepsis
Treatment: antibiotics
150
Q

Chronic pyelonephritis?

A

Result in recurrent episodes of acute pyelonephritis
Need predisposition such as vesicouretal reflux
Chronicically obstructing kidney stones
Coarse, asymetric corticomedullary scarring
Blunting of calyx
Tubules can contain eosinophillic casts resembling thyroid tissue

151
Q

What is xanthrogranulomatous pyelonephritis?

A

Rare

Widespread kidney damage due to granulomatous tissue containy foamy macrophages.

152
Q

What are causes of diffuse cortical necrosis?

A

Acute generalized cortical infarction of both kidneys
Likely due to combination of vasospasm and DIC

Usually associated with obstetric catastrophes (abruptio placentae and septic shock)

153
Q

Renal osteodystrophy?

A

Hypocalcemia
Hyperphospatemia
Failure of vitamin D hydroxylation associated with chronic renal disease

Secondary hyperphospatemia causes:
Decrease in Ca by causing tissue calcification where 1.25 OH D2
Decrease intestinal Ca 2+ absorption
C

154
Q

Characteristics of acute kidney injury?

A

Abrupt decline in renal function by increasing creatinine and increassing BUN

155
Q

What is prerenal azotemia?

A

Due to decrease in renal blood flow
Decrease in GFR
Na/H2O and BUN retained by the kidney in an attempt to conserve volume

Increase BUN/Creatinne ratio
BUN is reabsorbed (creatinine is not)

Decrease in FeNa

156
Q

What is intrinsic renal failure?

A

Due to acute tubular necrosis or ischemia/toxins
Less commonly due to acute glomerulonephritis (RPGN, hemolytic uremic syndrome) or acute intersitital nephritis

In ATN, patchy necrosis (debris obstructing tubule and fluid backflow)

Urine has epthielial/granular casts
BUN resorption is impaired

Decreasein BUN/creatinine ratio

157
Q

Characteristics of postrenal azotemia?

A

Due to outflow obstruction
(stones, BPH, neoplasia, congenital abnormalities)
Due to bilateral obstruction

158
Q

Please compare the different types or acute kidney injury and describe the urine osmolarity, urine Na, FeNa, Serum BUN/Cr?

A

Pre-renal Intrinsic Renal Post Renal
Urine osmolarity >500 < 350 <350
Urine Na <20 >40 >40
FeNA <1% > 2% >1% mild
> 2% severe
Serum BUN/CR >20 <15 Varies

159
Q

Consequences of renal failure?

A 
Inability to make urine and excrete nitrogenous waste 
Metabolic acidosis
Dyslipidemia 
Hyperkalemia
Uremia (clinical syndrome marked by increased BUN)
Nausea and anorexia 
Pericarditis
Asterixis
Encephalopahty
Platelet dysfunction

Na/H2O retention (HF and pulmonary edema)

160
Q

Characterstics of acute interstitial nephritis

A

Acute interstitial renal inflammation

Pyuria
Asotemia
After the adminsitration of drugs that act with hypersensitivity

(Drugs implicated inclute diuretics, penicillin, propton pump inhibitor, sulfonamides, rifampin, NSAUDS

Secondary processes:
systemic infection *mycroplasma) 
Autoimmune
SLE
Sarcoidosis
161
Q

Characteristics of acute tubular necrosis ?

A

Most common cause of acute kidney injury in patients
Can resolve spontaneous or be fata (especially in oliguirc phase)

Has increased FeNa

162
Q

3 stages of acute tubular necrosis?

A
  1. Inciting event
  2. Maintenence phase (oliguric) lasts 1-3 weeks
    risk of hyperkaliemie
    Metabilic acidosis
  3. Recovery phase: polyuric, hypokalemia,
163
Q

Causes of acute tubular necrosis?

A

Ischemicsecondary to decreased renal blood flow (hypotension, shock, spsis, hemorrahe, HF)

Results in death of the tubular cell
PCT is especially painful

Nephrotoxic:
Secondary to injury from toxis substances (aminoglycosides, radiocontrast agents, lead, cisplatin, cush injury)

164
Q

Characteristics of renal papillary necrosis?

A

Sloughing off of necrotic renal papillae
Gross hematuria and protinuria
May be due to recent infection or immune stimulus

Usually associated with sickle cell disease of trait
Acute pyelonephritis
NSAIDS
DM

165
Q

Characteristics of autosomal polycystic kidney disease?

A

Numerous cysts in the cortex and medulla
Bilateral enlarged kidneys
Destroys the kidney parenchyma

Presents with flank pain, hematuria, HTN, urinary infection

Leads to progressive kidney failure in 50% of the patients

166
Q

What are the mutations from polycystic kidney disease?

A

PKD1 or PKD2

Death from disease of the kidney disease, or HTN

167
Q

what are polycystic kidney disease associated with?

A

Berry aneurysm
Mitral valve prolapse
benign hepatic cysts

168
Q

Treatement of polycystic kidney?

A

ACE or ARB

169
Q

Characteristics of autosomal recessive polycystic kidney disease?

A

Cystic dilatation of the collecting ducts
Presents within infancy
Associated with congenital hepatic fibrosis
Signigicant oliguirc failure in utero can cause Potter sequence
Beyond neonatal peropd can have systemic hypertension, progressive renal insuggiciency
Portal HTN
HTN with congential fibrosis

170
Q

Characteristics of medullary cystic disease?

A 
Causes tubulointerstitial fibosis
Renal insufficency with inability to concentrate urine 
Medullary cysts not visualized
Have shrunken kidneys on ultrasound
Poor prognosis
171
Q

Simple vs complex cysts?

A

Simple Are filtered with ultrafiltrate (anechoic on U/S), usually assymptomatic and beningn

Complex cysts: have septations, enahnced, with solid components on imaging. Need follow up.
Have an increased risk of renal cell carcinoma.

172
Q 
Site of action of diuretics?
Mannirol
Acetazolamide
Loop diuretics
Thiazide
K sparing?
A 
Mannitol: proximal 
Acetazolamide:proximal 
Loop: ascencding loop of Henle
Thiazid: Distal convoluted
K sparing: collecting
173
Q

Mechanism, clinical use, adverse effects of mannitol?

A

Osmotic dures
Increase fluid osmolarity
Increase in urine flow
Decrease intracranial and intraocular pressure

Clinical use: drug overdose, elevated intracranial/intraocular pressure

Advers: pulmnar edema, dehydration, contraindicated in anuria and HF

174
Q

Clinical, adverse, mechanism of azetazolamide?

A

Carbonic anhydrase inhibitors
Causes self limited NaHCOs diuresis
Decrease total HCO3 stores

Clincial uses:
Glaucoma
Urinary alkalinization, metabolic alkaslosis
Altitude sickness
pseudotumor cerebri.

Adverse: proximal renal tubular acidosis
Parestheisis
NH# toxicity
Sulfa allergy

175
Q

Clinical, Adverse and mechanism of loop diuretics (Gurosamide, bumetanide, torsemide?)

A

Mechanism:inhibit Na/k/Cl of ascending limb of loop of Henle

Abolish hypertonicity of medulla
Prevents concentration of urine

Stimulares PGE release: vasodilatory effect on afferent arteriole

Inhibited by NSAIDS

Increase Ca excretion (CA wasting)

Clinical: edema, cirrhosis, HF, nephotic syndrome

Adverse effects: 
Ototoxicity
Hypokalemia
Dehydration 
Allegery (sufla)
Metabolic Alkalosis
Nephritis
Intersitial 
Gout
176
Q

Clinical, adverse, of ethacrynic acid?

A

mechanims: inhibits the Na/K/2Cl of ascending
Clinical use: diuresis in patients allergic to sulfa
Adverse: similar to lasix but more otototoxic.

177
Q

Clincial, adverse, mechanism of Thiazide diuretics?

A

HCTZ, chlorthalidone, metalazone

Mechanism: inhibits Nacl resoprtion in DCT, decreases the diluting capacity of a nephron, decrease in Ca excretion

Clinical use: HTN, HF, idiopathic hypercaliuria, nephrogenic diabtetes, osteoporosis

Adverse effects: hypokalemia
Hyponatremia 
Hyperglycemis 
Hyperlipidemia
Hyperuricemia 
Hyper calemia 
Sulfa allergy
178
Q

Clinical, adverse of potassium sparing diuretics?

A

(spironolactone, epleronn, traimenterne, amiloride)

Mechanism: they are competitive aldosteron receptorantagonists

Clinical use: hyperadlsoterone
K depletion 
HF
Hepatic ascites
nephorgenic DI (amiloride)

Adverse effetcs: hyperkalemia leasing to arrythmias
Endocring effects with spironalactone
Gynecomastia
Anti-androgen effects.

179
Q

What are changes with diuretics (electrolyte changes)

A

Urine NaCl; increase with all diuretics
Urine K: increase with loop diuretics and thiazide diuretics (serum K may decrease)

Blood pH Decrease acidemia (carbonic anhydrase inhibitors) decrease HCO3 resoprtion
Ksoaring
blockade prevents K and H secretion
Additionally hyperkalemia leads to to K entering the cells

Increase alkalemia
K loss through K+ exiting all cells
In low K state, H is exchanged for Na+ in cortical collecting tubule (alkalsosi and paradoxical aciduria)

Urine Ca decreases leading to hypocalcemia

180
Q

How do ACE inhibitors work?

A

(captopril, enalapril, lisinopril, ramipril)

Mechanism: inhibit ACE and decrease AT 2 and decrease GFR

Prevents constriction of efferent arterioles
Increase in renin due to loss of negative feedback
Inhibition of ACE prevents inactivation of bradykinin (therefore, it is vasodilator)

Clinical use: HTN, HF, protienuria, diabetic nephropathy

Adverse: cough, angioedema, teratogen, increase creatinine, , hyperkalemia, hypotension

181
Q

Angiotensin 2 receptor blockers?

A

Losartan, candsartan, valsartan
Mechaism: slectively binds to angiotensin II to At receptor

Effect is similar to ACE inhibitors
ARBS do not increase bradykinin

Clinical uses: HTN, HF, proteinuria, diabetic nephorpathy with intolerance to ACE inhibitors,cough, angioedema

Adverse effects: Hyperkalemia, decrease GFR, hypotension, teratogen

182
Q

Mechanism, clinical use, adverse effects of Aliskiren?

A

Mechanism: Direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin 1

Clinical use Hypertension

Adverse effects: Hyperkalemia
Decrease GFR
Hypotension
Relatively contraindicated in patients taking ACE

US (17 decks)

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