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Renal and GU Flashcards

1
Q

What is the definition for acute kidney injury based open?

A

Rapid decline in renal function with an increase in serum creatinine level

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2
Q

What are the criteria for the RIFLE definition of acute kidney injury?

A

RISK: 1.5x Cr OR -25% GFR OR urine output <0.5 for 6h
INJURY: 2x Cr OR -50% GFR OR uo <0.5 for 12h
FAILURE: 3x Cr OR -75% GFR OR uo <0.5/24 or anuria 12h
LOSS: complete loss of kidney function requiring dialysis for >4wks
ESRD: dialysis >3mo

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3
Q

What are the most common clinical symptoms of acute kidney injury? Why?

A
  1. Weight gain
  2. Edema
    Both due positive water and sodium balance
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4
Q

What are some common causes of azotemia (increase in BUN, increased in Cr)?

A

BUN: catabolic drugs (steroids), GI/soft tissue bleeds due to RBC digestion and re-absorption of urea, dietary protein intake

Cr: increased muscle breakdown, various drugs. Baseline may vary with difference in muscle mass

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5
Q

What are the most common causes in morbidity in acute kidney injury?

A

Infection (75%)

Cardiorespiratory complications

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6
Q

What are (3) common causes of pre-renal acute kidney injury?

A
  1. Volume loss/sequestration
  2. Decreased cardiac output
  3. Hypotension
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7
Q

What are (4) common causes of intra-renal acute kidney injury?

A
  1. Glomerulonephritis
  2. Vascular disorder (small, large vessel)
  3. Interstitial disorder
  4. Acute tubular necrosis
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8
Q

What are the common causes of post-renal acute kidney injury?

A

Intrarenal: crystals, proteins
Extrarenal: pelvis/ureter, bladder/urethra

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9
Q

What physical exam parameters need to be evaluated daily to monitor for acute kidney injury progression?

A
  1. Daily weights, I/O
  2. BP
  3. Electrolytes
  4. Hb, Hct
  5. Infection signs
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10
Q

Presentation of a patient with signs of water depletion and CHF or cirrhosis would suggest acute kidney injury of which etiology?

A

Pre-renal

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11
Q

Presentation of a patient with signs of an allergic reaction (rash) would suggest acute kidney injury of which etiology?

A

Intra-renal: acute interstitial nephritis

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12
Q

Presentation of a patient with a suprapubic mass, BPH, or bladder dysfunction suggest acute kidney injury of which etiology?

A

Post-renal

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13
Q 
For a pre-renal cause of acute kidney injury, what would lab values for the following usually show?
UA
BUN:Cr ratio
FENa
Urine osmolality
Urine sodium
Urine sediment
A

UA: hyaline casts
BUN:Cr: >20:1 (GFR is decreased so filtration of metabolites is decreased, but tubules increase urea reabsorption to help reabsorb Na and H2O)
FENa: <1%
Urine osmolality: >500mOsm (tubular function is preserved so water is reabsorbed)
Urine sodium: <20 (tubular function is fine so electrolytes can be reabsorbed)
Urine sediment: scant (indicates lack of tubular damage)

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14
Q 
For a intra-renal cause of acute kidney injury, what would lab values for the following usually show?
UA
BUN:Cr ratio
FENa
Urine osmolality
Urine sodium
Urine sediment
A

UA: abnormal
BUN:Cr ratio: <20:1 (tubules cannot actively reabsorb urea since they are damaged)
FENa: >2-3% (Na not effectively reabsorbed)
Urine osmolality: 250-300mOsm (damage to tubules creates difficulty in concentrating urine)
Urine sodium: >40
Urine sediment: full, brownish pigment // granular casts with epithelial casts

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15
Q

What are some common causes of intrinsic renal damage?

A

Tubular disease: ischemia, nephrotoxins
Glomerular disease: Goodpasture, GPA, PSGN, lupus
Vascular disease: renal artery occlusion, TTP, HUS
Interstitial disease: allergic interstitial nephritis (usually due to hypersensitivity medication)

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16
Q

What are some common nephrotoxins that may lead to intrinsic renal disease?

A

Antibiotics (aminoglycosides, vancomycin)
NSAIDs
Poisons
Myoglobinuria (muscle damage, rhabdomyalysis)
Hemoglobinuria (from hemolysis)
Chemo drugs (cisplatin)
Kappa, Gamma light chains (multiple myeloma)

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17
Q

What are the (3) basic tests to evaluate for post-renal kidney failure?

A
  1. Physical exam - palpate the bladder
  2. US - look for obstruction, hydronephrosis
  3. Catheter - look for large volume of urine
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18
Q

What are the (3) phases of acute tubular necrosis?

A
  1. Oliguric phase - azotemia and uremia (10-14d)
  2. Diuretic phase - fluid overload (due to retained solutes), or osmotic diuresis, or tubular damage
  3. Recovery phase
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19
Q

What lab tests are indicated in the diagnosis of acute kidney injury?

A 
Blood tests: BUN:Cr, e-, albumin, CBCd
Urinanalysis: protein, microscopic sediment
Urine chemistry: osmolality, FENa
Urine culture/sensitivities
Renal US: obstruction
CT abdomen, pelvis: if US abnormal
Renal arteriography: RA occlusion
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20
Q 
What do the following findings in urine microscopy indicate about the etiology of kidney damage?
Crystals
Micro-organisms
Granular casts
Hyaline casts
RBC casts
WBC casts
Fatty casts
A

Crystals: stones
Micro-organisms: infection, nonpathogenic colonization
Granular casts: “muddy brown,” seen in ATN due to degeneration of cells and protein aggregates
Hyaline casts: “empty,” prerenal injury
RBC casts: glomerular disease
WBC casts: renal parenchymal inflammation
Fatty casts: nephrotic syndrome

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21
Q

What intrinsic renal disease is suspected if the UA results show “muddy brown” casts, renal tubular cells/casts, granular casts, with trace protein and no blood?

A

Acute tubular necrosis

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22
Q

What intrinsic renal disease is suspected if the UA results show dysmorphic RBC, RBC casts, WBC casts, fatty casts, with high protein and blood content?

A

Acute glomerulonephritis

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23
Q

What intrinsic renal disease is suspected if the UA results show RBCs, WBCs, WBC casts, eosinophils, with mild protein and blood?

A

Acute interstitial nephritis

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24
Q

What are (4) common complications of acute kidney injury and how are they treated?

A
  1. ECF volume expansion w/pulmonary edema // treat with diuretic (furosemide)
  2. E- abnormalities (hyperK, metabolic acidosis // NaHCO2, hypoCa, hypoNa, hyperPO4, hyperurecimia)
  3. Uremia
  4. Infection
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25
What are the indications for urgent dialysis in acute kidney injury?
``` Acidosis Electrolytes Intoxications Overload in volume Uremia ```
26
What fluid replacement is given normally? What if acidemia is present?
Usually normal saline | If acidemia, use lactated ringers due to risk of hyperCl
27
Why does radiographic contract cause ATN? How can it be prevented?
Contrast dye causes afferent arteriole spasms; can pre-treat with saline hydration
28
What measurements define chronic kidney disease?
GFR <60, or structural/functional abnormalities for >3 months
29
What are the (2) main causes of CKD? What are some other causes?
1. Diabetes (30%) 2. HTN (25%) 3. Chronic glomerulonephritis 4. Interstitial nephritis, PCKD, obstructive uropathy 5. Prolonged AKI leading to CKD
30
What is the most common clinical measure of GFR?
Cr clearance
31
``` What are the clinical symptoms of CKD? Neurologic CV GI Hematologic Endocrine/metabolic ```
Neurologic: lethargy, somnolence, confusion, peripheral neuropathy, uremic seizures, weakness, asterixis, hyperreflexia, restless legs, hypoCa sx (lethargy, confusion, tetany) CV: HTN (2/2 Na+H2O retention - decreased GFR leads to increased RAAS, BP), CHF (volume overload, anemia), pericarditis (uremia) GI: (usually due to uremia) n/v, anorexia Hematologic: normocytic normochromic (2/2 EPO deficiency), bleeding (2/2 platelet dysfunction due to uremia) Endocrine/metabolic: hyperPO4, hypoCa, hyperPTH leading to renal osteodystrophy, CaPO4 crystals causing calciphylaxis (irreversible)
32
What is the prognosis of CKD if small kidneys are seen on renal US?
Chronic renal insufficiency with small chance of recovery
33
What (10) factors does a treatment plan for CKD need to include?
1. Diet: low protein, low salt, restrict K, Ph, Mg 2. ACEi - slows proteinuria, but may lead to hyperK 3. BP control 4. Glycemic control 5. Smoking cessation 6. Correct e- 7. Anemia - (+) EPO 8. Pulmonary edema (diuresis, dialyze if needed) 9. Pruritis - capsaicin cream, cholestyramine, UV light 10. Dialysis
34
What is the only cure for CKD?
Transplant
35
What are the two types of dialysis available?
Hemodialysis | Peritoneal dialysis
36
What are the absolute indications for dialysis? (Hint: there is a mnemonic)
``` A: acidosis E: electrolyte abnormalities I: intoxication O: overload, volume U: uremia ```
37
What are the symptoms of uremia?
Neurological: lethargy/deterioration in MS, encephalopathy, seizures CV: pericarditis GI: nausea, vomiting
38
What are the benefits and risks of hemodialysis?
Benefits: more efficient with high flow rates that shorten dialysis time, can be initiated quickly with temporary catheter sites Risks: dissimilar to natural kidney function, rapid volume exchange may cause HPN leading to rapid shift of fluid from ECF into cells, hypoOsm due to solute removal, requires vascular access
39
What are alternatives to traditional hemodialysis? When are they used?
CAVHD: continuous arteriovenous HD CVVHD: continuous venovenous HD - used in hemodynamically unstable patients (i.e. ICU patients with AKI)
40
What are the benefits and risks of peritoneal hemodialysis?
Benefits: mimics natural kidney function since it is continuous, patients can do it themselves Risks: high Glu may cause hyperGly and hyperTG, peritonitis, requires patients to take responsibility for use, abdominal distention
41
Although dialysis can replace some kidney function, what properties of the kidney can it not replace?
Kidneys' synthetic functions: EPO production, vitamin D activation
42
What is "first-use syndrome" in relation to hemodialysis?
Reaction to using a new dialysis machine leading to chest pain, back pain, and rarely, anaphylaxis
43
What MSK syndrome may arise due to hemodialysis use? Why?
BL Carpal Tunnel Syndrome: hemodialysis-associated amyloidosis of B2-microglobulin in bones and joints
44
What is the laboratory cutoff for proteinuria?
>150mg/protein/24h
45
What are the (3) main categories of proteinuria? Why do they occur? What are some causes of each?
1. Glomerular: increased permeability may lead to nephrotic syndrome; loss may be more severe than other causes of proteinuria (causes: glomerular nephritis) 2. Tubular: decreased reabsorption of small proteins; kidney damage is less severe since nephrotoxicity of proteins is usually less (SCD, UTO, interstitial nephritis) 3. Overflow: increased production overwhelms kidney ability to reabsorb (multiple myeloma - Bence Jones protein, rhabdomyolysis - myoglobin)
46
What are some other causes of proteinuria not directly related to kidney pathology?
``` UTI Fever Heavy exertion/stress CHF Pregnancy Orthostatic proteinuria ```
47
What are the (3) key features of nephrotic syndrome? Why does it occur?
1. Proteinuria : glomerular, tubular, overload, other 2. HypoALB: hepatic production cannot keep up with losses 3. HyperLPD: increased hepatic LDL/VLDL production due to increase in attempt to produce albumin
48
Why is there an increased risk in infection with nephrotic syndrome? Infections caused by which organism are most prominent?
Loss of immunoglobulins as part of small protein loss; pneumococcal
49
When urine dipstick analysis is used for diagnosis of proteinuria, what is one limitation of what it tests for?
Specific to albumin, so proteinuria due to globulin loss (like multiple myeloma) may be missed
50
After UA confirms the presence of protein, what test is indicated next?
24h urine collection to determine significance of protein loss
51
What may be the earliest sign of diabetic nephropathy but overt signs and symptoms may be seen?
Microalbuminuria
52
What immunologic tests may be indicated when determining the etiology of proteinuria?
``` ANA: lupus Anti-glomerular BM: Goodpasture Hepatitis serology: MN, MPGN Antistreptococcal AB: PSGN Complement levels Cryoglobulin studies ```
53
What is an essential medication in treating diabetics with HTN who show symptomatic proteinuria? Why?
ACEi - decrease urinary albumin loss
54
What does microscopic hematuria suggest about the etiology of bleeding? What about gross hematuria?
Microscopic: more likely glomerular in origin Gross: nonglomerular or urologic
55
What is the assumption when gross painless hematuria is reported?
Assume bladder or kidney cancer until proven otherwise
56
What are common causes of hematuria in the following locations? Intrarenal Ureter Lower urinary tract (bladder, urethra, prostate) Other
Intrarenal: tumor, infection, stones, trauma, glomerular dz, IgA nephropathy, strenuous exercise, fever, PCKD, cysts, SCD, analgesic induced, renal papillary necrosis Ureter: tumor, infection, stones, trauma, stricture Lower urinary tract (bladder, urethra, prostate): tumor, infection, stones, trauma, BPH, chronic irritation Other: systemic diseases (SLE, HSP, rheumatic fever, GPA, HUS, GP, PAN), bleedign disorders, medications
57
What medications may lead to hematuria?
Cyclophosphamide Anticoagulants Salicylates Sulfonamides
58
What test has 90%+ sensitivity in detecting hematuria?
Urine dipstick
59
When evaluating hematuria, what is the next step after UA shows normal-shaped RBCs, no casts, no proteinuria, with NEG UCx? What happens if the next evaluation is NEG?
Evaluate for coagulopathy | If neg, do KUB to check for stones
60
What evaluating hematuria, what is the next step if UA shows pyuria with a POS UCx?
Treat UTI and reevaluate
61
When evaluating hematuria, what is the next step after UA shows dysmorphic RBCs, RBC casts, or proteinuria?
Evaluate for intrinsic renal disease with serology, 24h urina, GFR, renal bx
62
What is the next step after sending a urine specimen for cytology if the suspicion for malignancy is high?
Cystoscopy, especially if patient is 40+ with RF for bladder cancer
63
``` Regarding nephrotic syndrome: Pathophysiology? Causes? Lab findings? Clinical symptoms? ```
Pathophysiology: increased glomerular permeability Causes: MG (mc), DM, SLE, infection, drugs, GN Lab findings: urine protein >3.5g/d, hypoalbuminemia, HLD, fatty casts in urine Clinical symptoms: edema, hypercoagulable state, increased infection risk
64
``` Regarding nephritic syndrome: Pathophysiology? Causes? Lab findings? Clinical symptoms? ```
Pathophysiology: inflammation of glomeruli Causes: PSGN (mc), any cause of GN Lab findings: hematuria, AKI (azotemia, oliguria), mild proteinuria Clinical symptoms: HTN, edema
65
``` What is the most common cause of nephrotic syndrome? What population is is more common in? Pathophysiology? Microscopy findings? Prognosis? Treatment? ```
Minimal change disease, seen in children (asso w/Hodgkins and NHGD lymphoma) Pathophys: systemic T-cell dysfuction Light microscopy: nothing Electron microscopy: fusion/effacement of foot processes Good prognosis Treat with steroids
66
``` Pathophysiology of focal segmental glomerulosclerosis? Population? Clinical symptoms? Prognosis? Treatment? ```
Path: Histopathologic lesions with multiple causes Pop: 25% of nephrotic syndrome, common in blacks Sx: hematuria, HTN Prognosis: poor; renal insufficiency in 5-10 yrs, ESRD Tx: controversial - cytotoxic agents, steroids, immunosuppressive agents, ACE/ARBs
67
``` Pathophysiology of membranous glomerularnephritis? Population? Clinical symptoms? Prognosis? Treatment? ```
Path: thickened capillary walls, idiopathic (mc), infections (HCV, HBV, syphilis, malaria), drugs (gold, captopril, penicillamine), malignancy, lupus Pop: Non-diabetic adults Prognosis: fair to good, remission (40%), renal failure (33%) Tx: n/a, steroid resistant
68
``` What is the most common cause of glomerular hematuria? Cause? Clinical symptoms? Microscopy findings? Prognosis? Treatment? ```
IgA Nephropathy (Berger disease) Path: URTI Sx: asx recurrent hematuria/mild proteinuria; gross hematuria 1-3d after URTI; normal renal function E- Microscopy: mesangial IgA and C3 deposition Prognosis: good, preserved renal function, renal ins (25%) Tx: n/a, steroids unproven
69
What is hereditary nephritis? Clinical symptoms? Treatment?
??? Sx: hematuria, pyuria, proteinuria, high-frequency hearing loss without deafness, progressive renal failure Tx: n/a
70
``` What is the most common cause of nephritic syndrome? Pathophysiology? Clinical symptoms? What marker may be elevated? Prognosis? Treatment? ```
Post-streptococcal GN Path: occurs 10-14d after infection with GAS (B-hemolytic) of URT or skin Sx: hematuria, edema, HTN, low complement levels, proteinuria Marker: ASO Prognosis: self-limited w/great prognosis, may RPGN Tx: supportive (HTN, diuretics), steroids if severe case, abx unproven
71
``` What is the classic triad seen in goodpasture syndrome? Clinical symptoms? What occurs prior to kidney disease? Biopsy findings? Treatment? ```
Proliferative GN (crescentic), pulmonary hemorrhage, IgG antoglomerular BM-AB Sx: rapidly progressive renal failure, hemoptysis, cough, dyspnea Prior: lung disease precedes kidney disease by days-weeks Biopsy: linear immunofluorescence pattern Tx: plasmapheresis to remove circulating anti-IgG AB, cyclophosphomide, steroids may decrease new AB
72
What are HIV nephropathy: Clinical symptoms? Histopathology? Treatment?
Sx: proteinuria, edema, hematuria Histo: ~collapsing form of FSGS Tx: prednisone, ACEi, antiretroviral tx
73
What are some other causes of secondary glomerular disorders not covered yet?
``` Diabetic nephropathy HTN nephropathy Lupus Dysproteinemias SCD Nephropathy GPA PAN ```

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