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Clinical Medicine II > acute and chronic renal failure > Flashcards

acute and chronic renal failure Flashcards

1
Q

How should we approach renal disease

A
  1. Assess cause and severity (duration, UA, GFR)
  2. Pre/Post renal or intrinsic?
  3. Duration: acute (hr to d) or chronic (mo to yr)
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2
Q

UA should be examined when

A

w/in 1 hr collection

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3
Q

what does the dipstick measure

A 
specific gravity
pH
protein
Hbg
glu
ketones
bilirubin
nitrites
leukocyte esterase
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4
Q

What dose the UA microscopic exam measure

A 
crystals
cells
casts
organisms
*the "C's" and org
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5
Q

hematuria, RBC casts and mild proteinuria =

A

glomerulonephritis

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6
Q

Heavy proteinuria and lipiduria =

A

nephrotic syndrome

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7
Q

on a UA, WBC, WBC casts and slight proteinuria suggests

A

interstitial nephritis

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8
Q

UA: WBC casts suggests

A

pyelonephritis (usually fever too)

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9
Q

UA: pyuria suggests

A

UTI

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10
Q

what are the four reasons for proteinuria in the UA

A
  1. Functional: benign process ie illness/exercise
  2. Overproduction of filterable plasma pro
  3. Abnormality in glomerular basement membrane
  4. Tubular: damaged reabsorption of PT
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11
Q

Functional reason for proteinuria indicates

A

benign process such as illness or exercise

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12
Q

Bence Jones proteins (MM) found in UA is due to what cause of proteinuria? What follow up test should be done?

A

Bence jones = OVERPRODUCTION of FILTERABLE plasma proteins

*need to do UPEP

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13
Q

What does an abnormality in the glomerular basement membrane cause and what associated finding will you normally see

A

BM abnormality causes proteinuria

*see large ALBUMIN spike

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14
Q

Damaged reabsorption of PT is a Tubular condition that causes what finding in UA? What does this suggest?

A

UA: proteinuria

*suggests acute tubular necrosis (think drugs or hereditary metabolic disorders)

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15
Q

what is the number one reason for renal failure

A

acute tubular necrosis = #1 cause renal failure?? this was my note

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16
Q

what often causes acute tubular necrosis

A

drugs or hereditary metabolic disorders

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17
Q

false positives for Hematuria may be due to

A

vitamin C, beets, rhubarb (myoglobin, Hbg too?)

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18
Q

what percent of cases of Hematuria are due to renal causes

A

10%

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19
Q

What is GFR and how do you measure it

A

GFR = index of renal function

*measure by Creatinine clearance: 24 hr collection and plasma Cr on same day

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20
Q

with stable renal function, Cr production and excretion should be..?

A

EQUAL

production = excretion with healthy kidney

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21
Q

Causes of elevated serum Cr include

A

Ketoacidosis

Drugs: Ceph, ASA, Cimetidine, Bactrum

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22
Q

Conditions that decrease serum creatinine include

A

Advanced age
Cachexia
Liver disease

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23
Q

Besides GFR, what is another way to assess renal function

A

Urea

*product of liver protein catabolism that is filtered then 50% reabsorbed in nephron

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24
Q

what is a normal BUN:Cr ratio

A

10-15:1

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25
Q

increased BUN is seen in

A

*Dehydrration
GI bleed
steroid use
CHF

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26
Q

reduced BUN is seen in..

A

liver disease (liver dz causes low BUN and low Cr)

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27
Q

Ultrasound is used to look for what?

A
  1. Hydronephrosis
  2. PCKD
  3. Kidney size
  4. Postvoid bladder residuals

*hydronephrosis and cysts especially

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28
Q

IVP is used to look at what?

A

IVP –> views entire urinary tract

*requires contrast injection

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29
Q

When would you not want to perform an IVP on a pt

A

if. ..
1. DM, serum Cr >2
2. Chronic Renal Failure, serum Cr>5
3. MM (bence jones proteins already clogging up liver)

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30
Q

If you want to look at neoplasms in kidney or retroperitoneal space, what test should you go for

A

CT

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31
Q

CT is good for looking at

A

renal carcinoma

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32
Q

What does MRI look for in regards to Renal conditions

A

corticomedullary function in…

  1. glomerulonephritis
  2. hydronephrosis
  3. renal vascular occlusion

*MRI is used when CT is contraindicated due to contrast

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33
Q

Arteriography and venography are good for looking at

A

stenotic lesions, aneurysm, renal v thrombosis

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34
Q

Unexplained acute renal failure, proteinuria or lesions warrant what type of study?

A

Percutaneous needle biopsy! tissue is issue

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35
Q

Percutaneous needle biopsy is indicated in what conditions

A
  1. unexplained acute renal failure
  2. proteinuria
  3. lesions
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36
Q

Acute vs Chronic renal failure: TIME

A

acute: hr to d
chronic: m to yr

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37
Q

Acute vs Chronic renal failure: CR and BUN

A

acute: high Cr, normal BUN
Chronic: high Cr, high BUN

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38
Q

Acute vs Chronic renal failure: PROTEINURIA

A

acute: mild proteinuria
chronic: +proteinuria

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39
Q

Acute vs Chronic renal failure: PTH

A

acute: normal PTH
chronic: high PTH, high Ca, high AlkPhos

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40
Q

Acute vs Chronic renal failure: CBC

A

acute: normal CBC
chronic: anemia

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41
Q

Acute vs Chronic renal failure: kidney size

A

acute: normal size kidney
chronic: small kidney

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42
Q

Acute vs Chronic renal failure: FLUID OUTPUT

A

acute: sudden oliguria
chronic: gradual fluid retention

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43
Q

Acute vs Chronic renal failure: N/V

A

acute: acute N/V
chronic: N/V

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44
Q

s/sx of ACUTE renal failure include

A

N/V, Malaise and altered sensorium

  • may get pericardial effusion and hear friction rub
  • Rales potentially heard if fluid overload
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45
Q

What lab values are consistent with acute renal failure

A
  • SUDDEN increase in BUN or CR (usually just Cr)
  • Hyperkalemia with peaked T waves
  • potentially anemia due to decreased EPO
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46
Q

What is the most common cause of acute renal failure

A

prerenal azotemia

*due to renal hypoperfusion

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47
Q

If hypoperfusion (prerenal azotemia)persists, what is the result

A

ischemia –> intrinsic renal failure

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48
Q

What are reasons for hypoperfusion (causing prerenal azotemia)

A
  1. Decrease in intravascular volume (GI loss, pancreatitis, burns)
  2. Change in vascular resistance (sepsis, ACEI, NSAIDS, epi)
  3. Low CO (CHF, PE, arrhythmias)
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49
Q

what are some reasons for decrease in intravascular volume (related to decreased renal perfusion)

A

GI loss, pancreatitis, burns

50
Q

What are some reasons for changes in vascular resistance (related to decreased renal perfusion)

A

Sepsis,
ACEI,
NSAIDS,
Epinephrine

51
Q

What are causes of low CO (related to decreased renal perfusion)

A

CHF
PE
arrhythmias

52
Q

what is the key to prerenal azotemia

A

careful assessment of

  1. volume status
  2. drug usage
  3. cardiac function
53
Q

what are lab findings reflective of Prerenal azotemia

A

UA: volume depleted, tubular casts
High BUN:Cr

Urine Na low in volume depletion
Urine Na high in Acute tubular necrosis**

54
Q

Postrenal Azotemia is what related to renal failure

A

LEAST common cause (5%) but MOST important bc REVERSIBLE

*occurs when urinary flow is obstructed

55
Q

What are causes of Postrenal azotemia (urinary flow obstructed)

A
  1. Urethral obstruction
  2. Bladder dysfunction
  3. Obstruction in both ureters

MEN: BPH*, also anticholinergic drugs (sudafed, antihistamines), stones

56
Q

What are signs/sx of postrenal azotemia

A

lower abdominal pain or distended bladder

57
Q

what are lab values indicative of postrenal azotemia

A

High urine osm
Low urine sodium
High BUN:Cr

58
Q

What type of imaging should you do if you suspect Postrenal azotemia

A

bladder US or cath.. then if these are normal, consider CT or MRI

59
Q

Is postrenal azotemia reversible

A

yes

60
Q

What percent of renal failure is due to actual INTRINSIC renal failure

A

50%

*need to exclude pre/postrenal causes

61
Q

What causes Intrinsic renal failure

A

there are multiple causes

*85% due to acute tubular necrosis

62
Q

Acute TUbular Necrosis is responsible for 85% of intrinsic renal failure cases which comprise 50% of renal failure cases. What are the major causes of acute tubular necrosis?

A
  1. Ischemia

2. Toxin

63
Q

What are reasons for the ischemia that causes acute tubular necrosis (most common cause of intrinsic renal failure)

A

ischemia due to

hypotension, hypoxemia, dehydration, shock, sepsis

64
Q

What are reasons for toxin exposure

*cause of acute tubular necrosis

A

EXOGENOUS toxins: aminoglycosides (gentamicin, vancomycin), cephalosporins, cyclosporine (rejected transplant), radiographic contrast (esp in DM)

ENDOGENOUS toxins: Myoglobinuria (crush injury), HyperK+ and hyperphos (cell lysis), hemoglobinuria (hemolytic anemia or transfusion rxn), Bence Jones proteins (MM)

65
Q

How should you treat the hyperK and hyperphos (endogenous toxins in acute tubular necrosis)

A 
hydration
urine alkalinization (perhaps a CA inhibitor? - acetazolamide?)
66
Q

What are lab findings in acute tubular necrosis (intrinsic renal failure)

A

brown urine with pigmented granular casts

*may see hyperK and hyperpho

67
Q

How should you treat acute tubular necrosis

A

*avoid volume overload and hyperK
= Loop diuretics (Lasix)
= restrict protein

*dialysis if life threatening electrolyte abn, worsening acidosis and no response to diuretic tx

68
Q

what is the prognosis for a pt with acute tubular necrosis

A

Medical illness: 20-50% mortality
Surgical setting: 70% mortality

*logically, mortality increases with age and additional co-morbidities

69
Q

What is the most common cause of interstitial nephritis?

A

DRUGS (responsible for 70% of cases)
*PCN, ceph, sulfa, NSAIDS, allopurinol

infection (strep, CMV, histoplasmosis) are also causes of interstitial nephritis

70
Q

what are s/sx of interstitial nephritis

A

fever, rash, arthralgias

71
Q

A pt comes in with fever, rash, arthralgias and a history of strep infection and PCN use.. you suspect what and what lab results might confirm your ddx?

A

suspect this pt has INTERSTITIAL NEPHRITIS

Labs: peripheral blood EOSINOPHILIA
UA may show RBC, WBC and WBC casts
*Proteinuria if NSAID induced

72
Q

How should you treat the pt you diagnosed with interstitial nephritis

A
  1. remove offending agent (ie PCN, ceph, sulfonamide, NSAIDS, allopurinol)
  2. short term high dose Prednisone
    * good prognosis! :)
73
Q

what is the good news you can tell you pt with interstitial nephritis after telling them to stop their meds and start a short term high dose Prednisone

A

they have a good prognosis!

74
Q

Post infectious glomerulonephritis is associated with what pathogen and what are indications for this condition?

A

associated with group A beta hemolytic strep (GBS)

  • high ASO titer
  • cola colored urin
  • supportive tx
75
Q

What is the most common form of glomerulonephropathy in the US

A

IgA nephropathy (deposition of IgA in glomerulus)

76
Q

What population typically do we see IgA nephropathy? what is the typical CC?

A

Children, young adults
*cc: gross hematuria
may be associated with URI
(note: adults usually have microscopic hematuria)

77
Q

A 10 yr old pt comes in with hx of URI 2 wks ago and has gross asymptomatic hematuria, cola colored urine, RBC casts… You order a serum IgA because you suspect what?.. how do you confirm this dx?

A

IgA nephropathy glomerulonephritis

renal biopsy needed for confirmation (serum IgA is increased in 50% of pt)

78
Q

what prognosis can you give a pt dx with IgA nephropathy

A

33% clinical remission

40-50% progressive renal insufficiency :(

79
Q

what are causes of membranous nephropathy

A
  1. immune mediated (ie hep B, endocarditis, SLE, thyroiditis, cancer) *may need prednisone or tranplant
  2. amyloidosis (primary in kidney, progressise to end stage renal dz in 2-3 yr)
80
Q

In regards to immune mediated membranous nephropathy, if you see signs of nephrotic syndrome, what should you think?

A

think occult neoplasms of lung, stomach and colon

81
Q

what tx might immune mediated membranous nephropathy need

A

prednisone or transplant

82
Q

what is the fiver year survival for a pt with membranous nephropathy

A

<20% five year survival

83
Q

What 2 conditions are responsible over 50% of chronic renal disease, and which is the most common

A

DM or HTN

*DM more common

84
Q

What s/sx are consistent with chronic renal disease (*note: DM, HTN most common causes)

A
  • progressive over mo to yr
  • uremic fetor (fishy odor on breath bc ^BUN)
  • s/sx multi system
85
Q

in any patient with renal failure you should what?

A

identify and correct all possibly reversible causes

  1. UTI
  2. HTN
  3. CHF
  4. toxins
86
Q

In both acute and chronic renal failure, what lab findings do you see

A

elevated BUN and Cr

87
Q

What is diagnostic for chronic renal failure

A

ultrasound showing BILATERAL SMALL KIDNEYS is diagnostic for chronic renal failure

88
Q

what are some complications associated with chronic renal failure

A
  • HyperK+: due to endogenous causes (trauma, hemolysis) or exogenous (diet, ACEI, K sparing diuretics)
  • Metabolic Acidosis (bc limiting production of NH4
  • HTN: salt/ water retention
  • CHF: extracellular fluid overload
89
Q

complications of chronic renal failure

A

hyperK, metabolic acidosis, HTN, CHF

90
Q

how do you treat chronic renal failure

A
  • Restrict: Pro, Na, H20, K
  • Dialysis if:
  • uremic sx appear,
  • fluid overload unresponsive to diuretics,
  • refractory hyperK,
  • severe metab acidosis
  • neuro sx
91
Q

What is nephrotic syndrome

A

Urine protein >3.5 g/24 hr
albumin <3 g
peripheral edema (usually due to Na retention)

*proteinura, edema, hyperlipidemia

92
Q

What s/sx might you see in additional to gross proteinuria, edema and <3 g albumin in a pt with nephrotic syndrome

A
  • Dyspnea due to pulm edema, pleural effusions or ascites

* Hyperlipidemia due to increased hepatic production

93
Q

What are pt with nephrotic syndrome frequently associated with having

A

33% have systemic renal disease (DM, Amyloidosis, SLE)

94
Q

A pt has DM or amyloidosis, they develop nephrotic syndrome.. do you need to biopsy?

A

there is NO NEED for renal biopsy if DM or amyloidosis is cause of nephrotic syndrome

95
Q

how do you treat nephrotic syndrome

A
  • Mod protein restriction (avoid neg N balance)
  • Na restriction, probably thiazide or loop (higher dose if hypoalbumemia)
  • anticoagulation tx if serum albumin <2 g
96
Q

if serum albumin is less than 2 g (such as in nephrotic syndrome), what tx is needed and why?

A

anticoagulation tx due to losses of ATIII, Pro C and Pro S

97
Q

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

A

Diabetic nephropathy!

Type I DM carries 30-40% chance of nephropathy after 20 yr

98
Q

what should you always check in DM pt

A

MICROALBUMINURIA

99
Q

in a pt with diabetic nephropathy, what might help slow progression of nephropathy

A

strict glycemic control and HTN tx

*ACEI used in DM pt may increase GFR initially but with macroalbuminuria, GFR drops

100
Q

What are the types of tubulointerstitial disease and what causes them

A
  1. Acute tubulointerstitial dz: caused by toxins and/or ischemia
  2. Chronic Tubulointerstitial disease: caused by *obstructive uropathy, vesicoureteral reflux, analgesics or heavy metals
101
Q

In acute tubulointerstitial dz, what are the primary causes, what will the UA show, and what imaging should you order

A

Acute tubulointerstitial disease:
caused by toxin exposure or ischemia
*need US, CT and maybe MRI

102
Q

in Chronic tubulointersitial disease, what are the primary causes, which is the most common, and what is associated with that specific cause

A

Obstructive Uropathy, Vesicoureteral reflux, analgesics, heavy metals

  • most common is obstructive uropathy:
  • prostatic dz in men
  • bilateral ureteral calculi
  • cancer of cervix, colon or bladder
103
Q

what is Vesicoureteral reflux and who is it usually seen in?

A

kids

  • urine passing retrograde from bladder to kidney during void due to incompetent vesicoureteral sphincter
  • common cause of chronic tubulointerstitial disease
104
Q

how do pt with vesicoureteral reflux usually present

A

HTN, chronic UTIs
*need US or IVP

remember: vesicoureteral reflux is a common cause of chronic tubulointerstitial disease

105
Q

How do analgesics such as acetaminophen, ASA or NSAIDS (usually OD) cause chronic tubolointerstitial disease? what lab findings are associated and what study should you order

A

analgesics decrease medullary blood flow –> chronic tubulointerstitial disease

  • may see hematuria, mild proteinuria, polyuria or anemia
  • do IVP
106
Q

s/sx of chronic tubulointerstitial dz

A 
polyuria (bc damage to tubular area causing inability to concentrate urine)
HyperK (distal tubules become aldo resistant)
Hyperchloremic acidosis (reduced ammonia production)
107
Q

how should you treat chronic tubulointerstitial dz?

A

depends on cause

108
Q

what three US sonographic criteria must simple cysts meet to be benign

A

echo free, sharply demarcated with smooth walls, an enhanced back wall (good transmission)

109
Q

why must you do US or CT in pt found with cysts

A

to differentiate simple cysts from malignancy, abscess or PCKD

110
Q

how will renal cell carcinoma show on US

A

it enhances but is lower density than rest of parenchyma (hypodense?)

111
Q

Frequency, prognosis, CC for PCKD is?

A

PCKD is somewhat common
50% pt have ned stage renal disease by age 60
CC: abdominal or flank pain with hematuria

112
Q

PCKD pt may have hx of..

A

hx of UTI or stone

strong family hx and 50% time associated with HTN

113
Q

PE on PCKD will reveal

A

usually palpable kidneys

114
Q

how do you confirm PCKD dx

A

US that shows multiple cysts

115
Q

If PCKD pt presents with flank pain, fever and leukocytosis what should you suspect

A

infection of renal cysts

116
Q

what is MM

A

malignancy of plasma cells, presence of Bence jones protein in urine

117
Q

what dose MM cause in kidney

A

tubular toxicity and obstruction by Bence Jones proteins precipitating in tubules (endogenous acute tubular necrosis)

118
Q

What is interesting about the bence jones proteins in MM

A

bence jones protein is light chain which is not detected in urine dipstick

119
Q

How is sickle cell anemia damaging to kidneys and what is the primary manifestation

A

sickling of RBC in medulla causes stasis, hemorrhage and papillary infarct
*primary manifestation = proteinuria

120
Q

how does aging after GFR

A

after 40, GFR starts to decline

  • more adverse drug rxn in older population bc:
    1. altered volume of distribution
    2. altered drug half life
    3. altered elimination

Clinical Medicine II (8 decks)

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