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Renal 1 Flashcards

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1
Q

Renal tubular defects - types

A
  1. Fanconi syndrome
  2. Bartter syndrome
  3. Gitelman syndrome
  4. Liddle syndrome
  5. Syndrome of apparent minelocorticoid excess
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2
Q

Fanconi syndrome - pathophysiology / results in

A

Generalized reabsorptive defect in early proximal convoluted tubule –> increased amino acids, glucose, HCO3- and PO4- – Metabolic acidosis (proximal renal tubular acidosis)

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3
Q

causes of Fanconi syndrome

A
  1. hereditary defects (Wilson disease, tyrosinemia, glycogen storage disease, cystinosis)
  2. iscemia
  3. multiple myeloma
  4. nephrotoxins/drugs (expired tetracyclines, ifosfamide, cisplatin, tenofovir, lead poisoning)
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4
Q

Bartter syndrome - pathophysiology (and result in)

A

Reabsorptive defect in thick ascending loop oh Henle
–> affects Na+/K+/2CL- cotransporter –>
1. hypokalemia
2. metabolic alkalosis
3. hypercalciuria
LIKE LOOP DIURETICS

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5
Q

Gitelman syndrome - pathophysiology (results in)

A 
Reabsosptive defect in Distal convoluted tubule 
LIKE THIAZIDE
1. hypokalemia
2. hypomagnesia
3. metabolic alkalosis
4. hypocalciuria
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6
Q

Gitelman syndrome vs Barrter syndrome according to severity

A

Barrter is more severe

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7
Q

Liddle syndrome - pathophysiology

A

Gain of function mutation –> increased Na+ reabsorption in collecting tubules (high activity of epithelial channel)

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8
Q

situation that mimics Liddle syndrome

A

hyperaldosternism (but aldosterone is nearly undetectable)

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9
Q

Liddle syndrome –> ….. (result in)

A
  1. hypertension
  2. hypokalemia
  3. metabolic alkalosis
  4. low aldosterone
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10
Q

Liddle syndrome - mode of inheritance / treatment

A

AD

amiloride

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11
Q

Syndrome of Apparent Mineralocorticoid excess - pathophysiology

A

hereditary deficiency of 11β-hydroxysteroid dehydrogenase which normally converts cortisol (can activate mineralocorticoid receptors) to cortizone (inactivate on mineralocorticoid receptors) in cell containing mineralocorticoid receptors –> increased mineralocorticoid activity

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12
Q

Syndrome of Apparent Mineralocorticoid excess - manifestations

A
  1. hypertension
  2. hypokalemia
  3. metabolic alkalosis
  4. low serum aldosterone levels
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13
Q

P02, PCO2, HCO3-, ph - normal ranges

A

PO2: 75-105 mm Hg
PCO2: 33-44 mm Hg
HCO3-: 22-28 mEq/L
pH: 7.35-7.45

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14
Q

Winters formula?? is a formula used to evaluate

A

respiratory compensation in a metabolic acidosis

PCO2=1.5 (HCO3-) + 8 +/- 2

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15
Q

Winters formula - explanation

A

If measured PCO2 is bigger than predicted PCO2 –> concominant respiratory acidosis
If measured PCO2 is smaller than predicted –> concomitant respiratory alkalosis

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16
Q

Metabolic alkalosis - DDx

A
  1. loop diuretics
  2. vomiting
  3. antiacids
  4. hyperaldosteronism
  5. thiazide use
  6. Hypokalemia
  7. several renal tubular defects
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17
Q

Respiratory alkalosis - DDx

A

Hyperventilation:

  1. Hysteria
  2. Hypoxemia (eg. high altitude)
  3. Pulmoary embolism
  4. Tumor
  5. salicylates (early)
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18
Q

Respiratory acidosis - DDx

A

Hypoventilation:

  1. Airway obstruction
  2. Acute lung disease
  3. Chronic lung disease
  4. Opioids/sedatives
  5. weakening of respiratory muscles
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19
Q

Metabolic acidosis - next step

A

Check anion gap = Na+ - (CL+HCO3-):
more than 12 –> anion gap metabolic acidosis
8-12 –> normal anion gap metabolic acidosis

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20
Q

anion gap metabolic acidosis - DDx

A
  1. Methanol (formic acid)
  2. Uremia
  3. Diabetic ketoacidosis
  4. Propylene glycol
  5. Iron tablets
  6. ISONIAZIDE
  7. Lactic acidosis
  8. Ethylene glycol (–> oxalic acid)
  9. Salicilates (late)
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21
Q

normal anion gap metabolic acidosis - DDx

A
  1. Hyperalimentation (artificial supply of nutrients, typically intravenously)
  2. Addison disease
  3. Renal tubular acidosis
  4. Diarrhea
  5. Acetazolamide
  6. Spironolactone
  7. saline infusion
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22
Q

Renal tubular acidosis - types

A
  1. Distal tubular acidosis (type 1)
  2. Proximal renal tubular acidosis (type 2)
  3. Combined proximal and distal renal tubular acidosis (type 3)
  4. Hyperkalemic renal tubular acidosis (type 4)
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23
Q

Metabolic acidosis - predicted compensatory response

A

1 meq/L decrease in HCO3- –> 1.3 mmHg decrease in PCO2

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24
Q

Metabolic alkalosis - predicted compensatory response

A

1 meq/L increase in HCO3- –> 0.7 mmHg increase in PCO2

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25
Respiratory acidosis - predicted compensatory response
acute: 1 mmHg increase in PCO2 --> 0.1 meg/L increase in HCO3- chronic: 1 mmHg increase in PCO2 --> 0.4 meq/L increase in HCO3-
26
Respiratory alkalosis - predicted compensatory response
acute: 1 mmHg decrease in PCO2 --> 0.2 meq/L decrease in HCO3- chronic: 1mmHg decrease in PCO2 --> 0.4 meg/L decrease in HCO3-
27
Renal cell carcinoma - risk factors
1. Smoking 2. obesity 3. gene deletion of chromosome 3 (sporadic or inheritance as von Hippel-Lindau
28
Renal cell carcinoma - paraneoplastic syndromes
1. EPO 2. ACTH 3. PTHrP 4. RENIN
29
Renal cell carcinoma - prognosis? (why)
poor: 1. Resistant to chemotherapy and radiation therapy 2. Silent cancer --> comonly presents as a metastatic neoplasm
30
Renal oncocytoma - clinical manifestations
1. painless hematuria 2. flank pain 3. abdominal mass
31
Renal oncocytoma - treatment
often resected to exclude malignancy
32
Squamous cell carcinoma of the bladder - clinical manifestation
painless hematuria
33
Squamous cell carcinoma of the bladder - risk factors
1. Schistosoma haematobium infection (Middle East) 2. Chrinic cystitis 3. smoking 4. chronic nephrolithiasis
34
Transition cell carcinoma - manifestations
painless hematuria
35
Calcium oxalate stones are precipitated by (beside low ph)
1. ethylene glycol (antifreeze) ingestion 2. vitamin C abuse 3. malabsorption (Crohn disease) 4. hypocitraturia --> low ph
36
kidney calcium stone treatment
calcium oxalate --> thiazides, citrate, low-sodium diet | calcium phosphate --> thiazides
37
Ammonium magnesium phosphate stone (sturvite) are caused by
infection with urease + bugs (eg. Proteus mirabilis, Staphylococcus saprophyticus, Klebsiella) that hydrolize urea to ammonia --> urina alkalization
38
Ammonium magnesium phosphate stones (sturvite) - treatment
1. eradication of underling infection | 2. surgical removal of stone
39
Uric acid stones - risk factors
1. low sodium diet 2. alkalinization of urine 3. chelating agents if refractory
40
kidney stones - types and urine crystals
1. Calcium oxalate --> shaped like envelope or dumbbell 2. Caclicum phosphate --> wedge-shaped prism 3. Ammonium magnesium phosphate --> coffin lid 4. Uric acid --> Rhomboid or rosettes 5. Cystine --> hexagonal
41
Urinary incontinence - types
1. Stress incontinence 2. Urgency incontinence 3. Mixed incontinence 4. Overflow incontinence
42
urinary Stress incontinence - mechanism
Outlet incompetence (urethral hypermodility or intrinsic sphincteric deficiency --> leak with high intra-abdominal pressure (eg. sneezing, lifting)
43
urinary Stress incontinence - increased risk with
obesity vaginal delivery prostate surgery
44
urinary Stress incontinence - management
kegel exercise, weight loss. pessaries
45
urinary Urgency incontinence - mechanism
Overactive bladder (detrusor instability) --> leak with urge to void immediately
46
urinary Urgency incontinence - treatment
1. pelvic floor muscle strengthening (Kegel) exercise 2. bladder training (timed voiding, distraction and relaxation techniques) 3. antimuscarinics (oxybutynin)
47
Overflow incontinence - mechanism
incomplete emptying (detrusor underactivity - weak to emoty the bladder or outlet obstruction) --> leak with overfilling --> increased postvoid residual (urinary retention) on cathetirization or ultrasound
48
Overflow incontinence - treatment
``` catherterization relieve obstruction (α-blockers for BPH) ```
49
3 MCC of UTI (in order)
1. E. Coli 2. S. saprophyticus 3. Klebsiella pneumoniae
50
UTI - diagnostic markers
1. + leukocyte esterase --> WBC activity 2. + Nitrate test --> reduction of urinary nitrates by bacterial species (indicates gram (-) organism, esp E. coli) 3. + Urease test --> urease-producing bags (eg. Proteus, klebsiella)
51
acute renal failure (Acute kidney injury) - TYPES
1. Prerenal azotemia 2. Intrinsic renal failure 3. postrenal azotemia
52
Prerenal azotemia - urine osmolairty (mOsm/Kg), urine Na+ meq/L, FENa, Serum BUN/Cr
- urine osmolairty --> more than 500 - urine Na+ less than 20 - FENa less than 1% - Serum BUN/Cr >20
53
Intrinsic renal failure - due to
- acute tubular necrosis or ischemia/toxins | - less commonly due to acute glomerulonephritis (RPGN, hemolytic uremic syndrome) or acute interstitial nephritis
54
intrinsic failure - urine osmolairty (mOsm/Kg), urine Na+ meq/L, FENa, Serum BUN/Cr
- urine osmolairty --> less than 350 - urine Na+ more than 40 - FENa more than 2% - Serum BUN/Cr less than 15
55
postrenal azotemia - urine osmolairty (mOsm/Kg), urine Na+ meq/L, FENa, Serum BUN/Cr
- urine osmolairty --> less than 350 - urine Na+ more than 40 - FENa more than 1% (mild) or 2% (severe) - Serum BUN/Cr varies
56
Acute interstitial renal nephritis (tubulointesritital nephritis) - clinical presentation/findings
``` IT CAN BE ASYMPTOMATIC 1. Fever 2. rash 3. hematuria (casts) 4. costovertebral angle tenderness 5. pyuria (classically eosinophils) 6. azotemia 7. oliguria (days to weeks after the factor) RESULTS IN ACUTE RENAL FAILURE ```
57
causes of Acute interstitial renal nephritis (tubulointesritital nephritis)
1. drugs that act as haptens, inducing hypersensitivity (eg. diuretics, penicillin derivatives, PPIs, sulfonamides, rifampin, NSAID) 2. Systemic infections (eg. mycoplasma) 3. Autoimmune diseases (eg. Sjogren syndrome, SLE, sarcoidosis)
58
Acute interstitial renal nephritis (tubulointesritital nephritis) may progress to
renal papillary necrosis
59
renal papillary necrosis - symptoms/findings
1. gross hematuria 2. proteinuria 3. flank pain
60
causes of renal papillary necrosis
1. Sickle cell disease or trait 2. acute pyelonephritis 3. NSAID (or phenacetin) 4. DM 5. Acute interstitial renal nephritis May be triggered by recent infection or immune stimulus
61
MCC of acute kidney injury in hospitalized patients
Acute tubular necrosis
62
Acute tubular necrosis - prognosis
can be fatal, esp during initial oligurinc phase
63
Acute tubular necrosis - FENa
more than 2%
64
Acute tubular necrosis - key finding
granular (muddy brown) casts
65
Acute tubular necrosis - stages
1. inciting event 2. Maintenance phase - oliguric 3. Recovery phase - polyuric
66
Acute tubular necrosis - maintenance phase - risk for
1. hyperkalemia 2. metabolic acidosis 3. uremia
67
Acute tubular necrosis - Recovery phase - findings
BUN and creatinine fall
68
Acute tubular necrosis - recovery phase - risk for
hypokalemia
69
Acute tubular necrosis can be caused by .... (groups)
1. ischemic factors | 2. nephrotoxic factors
70
Acute tubular necrosis - nephrotoxic factors - mechanism
2ry to injury resulting from toxic substance (eg. aminglycosides, radiocontrasts agents, lead, cisplatin), crush injury (myoglobinuria), hemoglobinuria
71
Cast in urine - types
1. RBC casts 2. WBC casts 3. Fatty casts (oval fat bodies) 4. Granular ("muddy brown") casts 5. Waxy casts 6. Hyaline casts
72
RBC casts - seen in
1. glomerulonephritis | 2. malignant hypertension
73
WBC cast - seen in
1. tubulointerstitial inflammation 2. acute pyelonephritis 3. trasnplant rejection
74
Fatty casts (oval fat bodies) - seen in / associated with
Nephrotic syndrome | - Maltese-cross sign under polarized light
75
Granular ("muddy brown") vs waxy casts - seen in / cells
granular --> acute tubular necrosis waxy --> renal failure BOTH ACELLULAR
76
Hyaline casts - seen in / contain
nonspecific, can be normal finding, often in concentrated urine samples - protein (acellula)
77
Nomenclature of glomerular disorders - focal (characteristcs and example)
- less than 50% of glumeri are involved | - ex. focal segmental glomerulosclerosis
78
Nomenclature of glomerular disorders - diffuse (characteristcs and example)
- more than 50% of glumeri are involved | - ex. diffuse proliferative glumerulonephritis
79
Nephritic syndrome vs nephrotic syndrome according to mechanism
Nephritic syndrome --> GBM disruption | Nephrotic syndrome --> podocyte disruption --> barier impaired
80
Nephritic syndrome - symptoms and findings
1. Hypertension (salt secretion and periorbital edema) 2. increased BUN and creatinine 3. oliguria 4. hematuria (with RBCs in urine) 5. Proteinuria in Subnehrotic range (in severe cases may be in nephrotic range)
81
Nephritic syndrome - diseases?
1. acute poststreptococcal glomerulonephritis 2. Rapidly progressive glomerulonephritis 3. IgA nephropathy (Berger disease) 4. Alport syndrome 5. Membranoproliferative glomerulonephritis 6. Diffuse proliferative glomerulonephritis
82
Nephrotic syndrome - symptoms and findings
1. Massive proteinuria (>3.5g/day) with hypoalbuminemia (pitting edema in soft tissues) 2. hyperlipidemia (frothy urine with fatty casts) 3. edema 4. hypogammaglobulinemia (increased risk of infection) 5. loss of antithrombin III --> hypercoagulable state
83
Nephrotic syndrome - diseases (and if 1ry or 2ry)
1. focal segmental glomeulosclerosis (1ry or 2ry) 2. minimal change disease (lipoid nephrosis) (1ry or 2ry) 3. Membranous nephropathy (membranous glomerulonephritis) (1ry or 2ry) 4. Amyloidosis (2ry) 5. Diabetic glomerulonephropathy
84
Nephritic-nephrotic syndrome?
severe nephritic syndrome with profound GBM damage that may damages the glomerular filtration charge barrier (if damage to GBM is severe enougj to damage charger barrier) --> nephrotic-range proteinuria (>3.5g.day) and concominant features of nephrotic syndrome
85
Causes of Nephritic-nephrotic syndrome
can occur with any form of nephritic syndrome, but is most common seen with 1. diffuse proliferative glomerulonephritis 2. Membranoproliferative glomerulonephritis
86
Nephritic vs nephrotic vs Nephritic-nephrotic syndrome according to protein excreted per day
nephritic: Proteinuria in Subnehrotic range (less than in severe casees may be in nephrotic range nephrotic: Massive proteinuria (>3.5g/day) with hypoalbuminemia Nephritic-nephrotic syndrome: nephrotic-range proteinuria (>3.5g.day)
87
Acute poststreptococcal glomerulonephritis - age / when
Most frequently seen in children (may also occur in adults) | - 2-4 weeks after A streptococcal infection of of skin (impetigo) or pharynx
88
Acute poststreptococcal glomerulonephritis - treatment
resolves spontaneously
89
Acute poststreptococcal glomerulonephritis - lab
1. + strep titers/serologies 2. low complement levels due to consumption 3. LM: glomeruli enlarged and hypecellular 4. IF: (starry sky) granular appearance (lumpy-bumpy) due to IgG, IgM and C3 deposotio along GBM and mesangium 5. EM: subepithelial immune complex (IC) humbs
90
causes of Rapidly progressive (crescentic) glomerulonephritis
several diseases processes may result in this pattern 1. Goodpasture - anti-GBM + anti alveolar BM 2. Granulomatosis with polyangiitis (Wegener) - PR3-ANCA/c-ANCA 3. Microscopic polyangitis, Churg strauus - MPO-ANCA/p-ANCA 4. poststreptococcal glomerulonephritis 5. Diffuse proliferative glomerulonephritis
91
Rapidly progressive (crescentic) glomerulonephritis - image
LM: crescent moon shape --> consist of fibrin and plasma proetins (eg. C3b) with glomerular parietal cells, monocytes, macrophages IF: a. Goodpasture --> linear b. wegener, Microscopic polyangitis --> negative IF (Pauci-immune --> no IG/C3 deposotion) c. if PSGN or Diffuse proliferative glomerulonephritis --> granular
92
Rapidly progressive (crescentic) glomerulonephritis - treatment / prognosis
emergent plasmapheresis | poor prognosis
93
Diffuse proliferative glomerulonephritis - mechanism
due to SLE or membranoproliferative glomerulonephritis
94
Diffuse proliferative glomerulonephritis - image
LM - wire looping of capillaries EM: subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposotion IF: granular
95
IgA nephrpathy (Berger disasee) -mechanism/presentation
episodic gross hematuria that occurs concurrently with respiratory or GI tract infection (IgA is secreted by mucosal linings) --> IgA complex RENAL PATHOLOGY OF HENOCH-SCHONLEIN PURPURA
96
IgA nephrpathy (Berger disasee) - image
LM - mesangial proliferation EM - mesangial IC depositis IF - IgA-based IC deposits in mesangium
97
Alport syndrome - mechanism / mode of inheritance
Mutation in type IV collagen --> thinning and splitting of glomerular basement membrane MC X-linked dominant
98
Alport syndrome - manifestation
1. Eye problem (eg. retinopathy, lens dislocation) 2. glomerulonephritis --> isolated hematuria 3. sensorineural deafness
99
Alport syndrome - image
Basket-weave" appearance on EM
100
Mebranoproliferative glomerulonephritis (MPGN) - mechanism
``` type 1 --> 2ry to hepatitis B or C infection, May also be idiopathic type 2 (dense deposit disease) --> associated with C3 nephritic factor (autoantibody that stabilize C3 convertase) --> low serum C3 levels ```
101
Mebranoproliferative glomerulonephritis (MPGN) - prognosis
poor response to steroids --> progress to chronic renal failure
102
Mebranoproliferative glomerulonephritis (MPGN) type I - image
subendothelial immune complex (IC) deposits with granular IF tram track appearance on PAS stain and H&E stain due to GBM splitting caused by mesangial ingrowth
103
Mebranoproliferative glomerulonephritis (MPGN) type I vs type to according to location of deposits
type 1 --> subendothelial | type 2 --> intramembranous
104
MCC of nephrotic syndrome in children / treatment
Minimal change disease (lipoid nephrosis) | - excellent response to corticosteroids
105
Minimal change disease (lipoid necrosis) - image
LM - normal glomeruli, lipid may be seen in PCT cells IF - normal EM - effacement of foot process
106
MCC of nephrotic syndrome in African and Hispanics
Focal segmental glomerulosclerosis
107
causes of focal segmental glomerulosclerosis
1. Can be 1ry (idiopathic) 2. 2ry to other conditions --> a. HIV infection b. Sickle cell anemia c. heroin abuse d. massive obesity e. interferon treatment f. chronic kidney disease due to congenital malformations
108
focal segmental glomerulosclerosis - course and treatment
may progress to chronic renal disease | 1ry disease has incosistent response to steroids
109
focal segmental glomerulosclerosis - image
LM - segmental sclerosis and hyalinosis IF - often (-), but may be + for nonspecific focal deposits of IgM, C3, C1... EF - effacement of ffot process similar to minimal
110
MC cause of 1ry nephrotic syndrome in Caucasian adults
Membranous nephropathy (membranous glomerulonephritis)
111
causes of Membranous nephropathy (membranous glomerulonephritis)
1. primary (antibodies to phospholypase A2 receptor) | 2. 2ry to: a. drugs (eg. NSAIDs, penicillamine) b. infections (HBV, HCV) c. SLE d. solid tumors
112
causes of Membranous nephropathy (membranous glomerulonephritis) - course and treatment
may progress to chronic renal disease | 1ry disease has poor response to steroids
113
Membranous nephropathy (membranous glomerulonephritis) - image
LM - diffuse capillary and BM thickenning IF - granular (immune complex) EM - "spike and done" appearance with subepithelial deposits
114
nephrotic syndrome - amyloidosis - image
LM - congo red stain shows apple green birefringence under polairzed light due to amyloid deposition in the mesangium
115
MCC of end-stage renal disease in US
Diabetic glomerulonephropathy
116
Diabetic glomerulonephropathy - mechanism
Nonenzymatic glycosylation of GBM --> increased permeability, thickening Nonenzymatic glycosylation of efferent arterioles --> increased GFR --> mesangial expansion
117
HCV, HBV nephritis - types
nephrotic --> Membraous nephropathy (membranous glomerulonephritis) nephritic --> membranoproliferative glomerulonephritis
118
Lupus nephritis - types
nephritic - diffuse proliferative glomerulonephritis | nephrotic - membranous glomerulonephritis
119
MC nephropathy worldwide
IgA nephropathy (Berger disease)
120
glomerular disease with subepithelial deposits
1. Acute poststreptococcal glomerulonephritis | 2. Membranous nephropathy (membranous glomerulonephritis)

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