Renal Flashcards

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
Effect on GFR, RPF and FF decrease in plasma?
Increase in GFR No change RPF increase FF
26
Effect on GFR, RPF, FF with constriction of ureter?
Decrease in GFR No change in RPF Decrease FF
27
Effect on GFR, RPF, FF with dehydration?
GFR decreases RPf descreases Increase FF
28
Normal range of glucose in the plasma levelÉ
Range is 60-120 mg per dl | Glucose should be completely resorbed in proximal convoluted tubule by Na+/glucose
29
At what glucose level does the transporters become saturated?
200 mg/dl | (this is when glucosuria begins) when all of the transporters are saturated
30
What happens to glucose during pregnancy?
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
31
what does the proximal collecting tubule do?
``` Resorbs: Glucose Amino acids HCO3 Na Cl PO3 K H20 ```
32
What does thin descending loop of Henle show?
Passively resorbs H2O via medullary hyetonicity (makes urine hypertonic)
33
what does thick ascending loop of Henle show?
``` Reorbs: Na K Cl Mg and Ca ``` Does NOTabsorb H2O
34
early Descending collecting tubule?
Resorbs Na Cl Makes uring fully dilute (hypotonic)
35
what does the collecting tubule do?
``` Resorbs: Na K H+ regulated by aldosterone ```
36
Fanconi defect?
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
37
Barter syndrome?
Resorptive defect in thick ascending loop of Henle Autosomal recessive Affects Na/K/Cl Results in hypokalemia, and metabolic acidosis with hypercalciuria
38
Gitelman syndrome?
``` Resorptive defect NaCl in DCT Similar to lifelong thiazide diurectics Autosomal recessive Less severe then Barter syndrome Hypokalemia Hypomagneisum Metabolic alkalosis Hypocalciuria ```
39
Liddle syndrome?
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 ```
40
Syndrome of Apparent Mineralcorticoid excess?
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
41
Relative concentrations along proximal convoluted tubules?
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.
42
How does the Renin-Angiotensin-aldosterone system work?
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
43
Fucntion of renin?
Secreted by JG cells in response to decrease renal arterial pressure and increase renal sympathetic discharge
44
Angiotensin II
Affects barorecptors function Limits reflex bradycardia which would normally accompany the pressor effect Helps maintain blood pressure and volume
45
ANP and BNP?
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
46
What does ADH do?
Regulates osmolarity | Responds to low blood volume states
47
What does aldosterone do?
Primarily regulares osmolarity (responds to low blood volume state)
48
Functions of juxtaglomerular appararus?
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
49
Mechanisms that cause shift of K out of the cell, and cause hyperkalemia?
``` Digitalis (blocks the Na/K ATPase HyperOsmolairty Lysis of cells (crush inhury, rhabdomyolysis, tumor lysis syndrome Acidosis B Blocker High Blood sugar (insulin deficiency) ```
50
Process that shifts K into the cells causing hypokalemia?
Hypo-osmolarity Alkalosis B-Adrenergc (Na/K ATP ase) Insulin (Increases Na/ K ATPase)
51
effects of low/ high Na?
Low:Nausea, Malaise, stupor, coma and seizures | High serum concentration: irritability, stupor, coma
52
High/low K?
Low: U waves are flattened T waves on ECG High serum: wide QRS and peaked T waves on ECG, arrythmias, muscle weakness
53
High/Low Ca?
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
54
High/low Mg 2?
Low: Tetany Torsards Hypokalemia ``` High: Decrease in Deep tendon reflexes Lethargy Bradycardia Hypotension Cardiac arrest Hypocalcemia ```
55
High/low phosphate?
Low: Bone loss Osteomalacia (adults) Rickets (children) High: Renal stones Metastatic calcifications Hypocalcemia
56
What are features of Barter syndrome?
No change in blood pressure Increase plasma renin Increase in aldosterone Increase in urine Ca
57
What are the features of Gitelman syndrome?
``` No change in blood pressure Increase in plasma renin Increase in aldosteron Decrease in serum Mg Decrease in urine Ca ```
58
Features of Liddle Syndrome?
Increase blood pressure Decrease in renin Decrease in aldosterone
59
Features of SIADH?
Increase in blood pressure Decrease in plasma renin Decrease in aldosterone
60
Primary hyperaldosterone (Conn syndrome)
Increase in blood pressure Decrease in plamsa renin Increase in aldosterone
61
Features of Renin-secreting tumor?
Increase in blood pressure Increase in plasma renin Increase in aldosterone
62
What is metabolic acidosis?
Decrease in pH Low Co2 Low HCO3 Compensation with hyperventilation
63
Metabolic alkalosis?
Increase in pH Increase in PCO2 Increase in HCO3 Compensation with hypoventilation
64
Respiratory acidosis?
Decrease in pH Increase in PCO2 Increase in HCO3 Increase renal absoprtion of HCO3 (resorption is delayed)
65
Respiratory alkalosis?
Increase in pH Decrease in PCO2 Decrease in HCO3 Compensatory: Decrease in renal HCO3 (resorption is delayed)
66
What are the steps of interpreting acid/base equations?
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
67
What are functions of erythropoeitin?
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
68
Function of caciferol?
Proximal collecting cells convert 25-OH vitamin D3 to 1.25-(OH)2 vitamin D3 (calcitriol, active form)
69
Functions of prostaglandins?
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
70
Functions of dopamine?
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
71
Function of parathyroid hormone on the kidney?
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) ```
72
What does aldosterone do?
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
73
what causes potassium out of the cell (causing hyperkalemia)?
``` Digitalis (blocks Na/ K/ ATP ase Hyperosmolarity Lysis of cells (crush injury, rhabdomyolysis) Acidosis B blocker High blood sugar (insulin deficiency) ```
74
What causes K to shift inside the cell (causes hypokalemia)?
``` Hypo-osmolarity Alkalosis B adrenergic agonist (increase in NA/K+ ATPase) Insulin (increase in Na+/K ATPase) Insulin shifts K+ into the cells ```
75
Low Na concentration?
``` Nausea Malaise Stupor Como Seizures ```
76
High Na concentration?
Irritability Stupor Coma
77
Low Ca concentration?
``` Tetanty Seizures QT prolongation Twitching Chovostek sign Spasm Trousseau's sign ```
78
High Ca concentration?
``` Stones (renal) Bones (pain) Groans (abdominal pain) Thrones (increase urinary frequency) Psychiatric overtones (anxiety, altered mental status) Not necessarily calciuria ```
79
Low magnesium concentration?
Tetany Torsades de point Hypokalemia
80
High Mg Concentration?
``` Decrease in deep tendon reflexes Lethargy Bradycardia Hypotension Cardiac Arrest Hypocalcemia ```
81
Low phosphate concentration?
Bone loss Osteomalacia (adults) rickets (children)
82
High phosphate concentration?
Renal stones Metastatic concentrations Hypocalcemia
83
Features of Barter Syndrome?
BP unchanged Increase plasma Renin Increase in aldosterone Increase in urine Ca
84
Features of Gitelman syndrome?
``` No change in blood pressure Increase in plasma renin Increase in aldosterone Decrease in serum MG Decrease in calcium ```
85
Features of Liddle syndrome?
Increase blood pressure Decrease plasma rernin Decrease aldosterone
86
Features of SIADH?
Increase BP Decrease plasma renin Decrease aldosterone
87
Features of primary hyperaldosterone (Conn)
Increase in BP Decrease in renin Increase aldosterone
88
Features of renin secreting tumor?
Increase BP Increase Renin Increase Aldosterone
89
Reaction to metabolic acidosis?
Hyperventilation (immediate)
90
Reaction to metabolic alkalosis?
Hypoventilation (immeditae)
91
Reaction to respiratory acidosis?
Increase in ranal HCO3 resoprtion
92
Reaction to respiratory alkalosis?
Decrease in renal absorption of HCO3 (delayed)
93
What is the formula to measure the respiratory compensation?
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
Causes of respiratory acidosis?
``` Airway obstruction Acute lung disease Chronic lung disease Opiods Sedatives Weakening of respiratory muscles ```
95
Causes of metabolic acidosis?
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
Causes of respiratory alkalosis?
``` Hyperventilation Hysteria Hypoxemia Salicylates Tumor Pulmonary embolism ```
97
Causes of metabolic alkalosis?
Loop diuretics Vomiting Antacid use Hyperaldosterone
98
Characteristics of distal renal tubular acidosis?
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
Proximal renal tubular acidosis (type 2)?
Urine pH less then 5.5 defect in HCO3 absoption Increased excretion of the HCO3 Associated with hypokalemia
100
Hyperkalemia renal tubular acidosis?
``` 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
what do casts in the urine symbolize?
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
what do RBC casys suggest?
Glomerulonephrotos | Malignant hypertension
103
what do WBC casts show?
Tubulointerstitial inflammation Acute pyelonephritis transplant rejectuon
104
what do fatty casts show?
Nephrotic syndrome (associated with Maltese Cross sign)
105
what does granular (muddy casts)
Acute tubular necrosis
106
what do waxy casts whow?
End stage renal disease /chronic renal failure
107
what do hyaline cases show?
Non specific Normal finding Seen in concentrated urine samples
108
Focal glomerular disease?
Less then 50% of glomeruli are involved | Focal segmental glomeruloscloerosis
109
Diffuse?
more then 50% of glomeruli involved | Diffuse proliferativ glomerulonephrites
110
Proliferative?
Hypercellular glomeruli | Membranoproliferative glomerlonephrities
111
Membraneous?
Thikcening of glomerular basement membrane (exapmle membraneous nephropathy)
112
Primary glomerular disease?
Primary disease of the kidney that affects the glomeruli | example: minimal change disease
113
What is Nephritic syndrome?
``` 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
What are the types of Nephritic syndrome?
``` Acute poststeptoccocal glomerulonephritis Rapidly progressive glomerulonephritis IgA nephropathy (Berger disease) Alport syndrome Membranoproliferative glomerulonephritis ```
115
What are characteristics of nephrotic syndrome?
``` 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
What are the types of nephortic syndrome?
``` Focal segmental glomerulosclerosis (1 or 2) Minimal change disease (1 or 2) Membraneous nephropathy (1 or 2) Amyloidois (2) Diabetic glomerulonephopathy ```
117
What are characteristics of nephritic-nephrotic syndrome?
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
what is the difference between the nephrotic and nephritic syndrome?
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
Nephritic syndrome characteristics?
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
Characteristics of acute poststreptoccal glomerulonephritis?
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
Characteristics of Rapidly Progressive (Concentric) glomerulonephritis ?
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
What is good pasture syndrome characteristics?
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
What are characteristics of diffuse proliferative glomerulnephritis ?
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
Characteristics of IgA nephopathy>
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
What are characteristics if nephritic syndrome?
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
what is minimal change disease?
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
What are characteristics of focal segmental glomerulossclerosis ?
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
Membranous nephropathy
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
Characterstics of Amyloidosis?
Congo stain will show apple green birfirengence Kidney is the most common involved organism Associated with chronic conditions that predispose to amyloid deposition
130
Characterstics of Diabetic glomerulonephropathy?
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
Kidney stone?
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
Type of stone: Calcium?
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
Ammonium magnsium phospahte stone?
``` 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
Uric acid kidney stones?
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
Cysteine stones?
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
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What is hydronephorsis?
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
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Renal cell carcinoma?
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
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Renal Oncocytoma?
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)
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Characteristics of Wilms Tumor?
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
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What is the WAGR complex? Deny-Drash syndrome? Beckwith-Wiedemann?
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
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What are characteristics of transitional cell carcinoma?
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
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Characteristics of squamous cell carcinoma of the bladder?
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
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List the 4 types of urinary incontinence?
Stress incontinence Urgency incontinence Mixed incontinene Overflow incontinence
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Characteristics of stress incontinence?
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
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Characteristics of urgency incontinence?
``` 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
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Mixed incontinence?
Features of both stress and urgency incontinence
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Characteristics of overflow incontinence?
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)
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Characteristics of urinary tract infection?
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)
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What are signs of acute pyelonephritis?
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 ```
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Chronic pyelonephritis?
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
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What is xanthrogranulomatous pyelonephritis?
Rare | Widespread kidney damage due to granulomatous tissue containy foamy macrophages.
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What are causes of diffuse cortical necrosis?
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)
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Renal osteodystrophy?
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
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Characteristics of acute kidney injury?
Abrupt decline in renal function by increasing creatinine and increassing BUN
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What is prerenal azotemia?
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
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What is intrinsic renal failure?
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
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Characteristics of postrenal azotemia?
Due to outflow obstruction (stones, BPH, neoplasia, congenital abnormalities) Due to bilateral obstruction
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Please compare the different types or acute kidney injury and describe the urine osmolarity, urine Na, FeNa, Serum BUN/Cr?
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
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Consequences of renal failure?
``` 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)
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Characterstics of acute interstitial nephritis
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 ```
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Characteristics of acute tubular necrosis ?
Most common cause of acute kidney injury in patients Can resolve spontaneous or be fata (especially in oliguirc phase) Has increased FeNa
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3 stages of acute tubular necrosis?
1. Inciting event 2. Maintenence phase (oliguric) lasts 1-3 weeks risk of hyperkaliemie Metabilic acidosis 3. Recovery phase: polyuric, hypokalemia,
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Causes of acute tubular necrosis?
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)
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Characteristics of renal papillary necrosis?
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
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Characteristics of autosomal polycystic kidney disease?
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
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What are the mutations from polycystic kidney disease?
PKD1 or PKD2 Death from disease of the kidney disease, or HTN
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what are polycystic kidney disease associated with?
Berry aneurysm Mitral valve prolapse benign hepatic cysts
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Treatement of polycystic kidney?
ACE or ARB
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Characteristics of autosomal recessive polycystic kidney disease?
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
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Characteristics of medullary cystic disease?
``` Causes tubulointerstitial fibosis Renal insufficency with inability to concentrate urine Medullary cysts not visualized Have shrunken kidneys on ultrasound Poor prognosis ```
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Simple vs complex cysts?
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.
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``` Site of action of diuretics? Mannirol Acetazolamide Loop diuretics Thiazide K sparing? ```
``` Mannitol: proximal Acetazolamide:proximal Loop: ascencding loop of Henle Thiazid: Distal convoluted K sparing: collecting ```
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Mechanism, clinical use, adverse effects of mannitol?
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
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Clinical, adverse, mechanism of azetazolamide?
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
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Clinical, Adverse and mechanism of loop diuretics (Gurosamide, bumetanide, torsemide?)
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 ```
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Clinical, adverse, of ethacrynic acid?
mechanims: inhibits the Na/K/2Cl of ascending Clinical use: diuresis in patients allergic to sulfa Adverse: similar to lasix but more otototoxic.
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Clincial, adverse, mechanism of Thiazide diuretics?
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 ```
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Clinical, adverse of potassium sparing diuretics?
(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.
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What are changes with diuretics (electrolyte changes)
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
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How do ACE inhibitors work?
(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
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Angiotensin 2 receptor blockers?
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
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Mechanism, clinical use, adverse effects of Aliskiren?
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